PKD Blog

Identification of Novel Mutations in Chinese Hans with Autosomal Dominant Polycystic Kidney Disease

2012-01-12T08:05:00.000-05:00

Identification of Novel Mutations in Chinese Hans with Autosomal Dominant Polycystic Kidney Disease
http://7thspace.com/headlines/402485/identification_of_novel_mutations_in_chinese_hans_with_autosomal_dominant_polycystic_kidney_disease.html

Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited renal disease with an incidence of 1 in 400 to 1000. The disease is genetically heterogeneous, with two genes identified: PKD1 (16p13.3) and PKD2 (4q21).

Molecular diagnosis of the disease in at-risk individuals is complicated due to the structural complexity of PKD1 gene and the high diversity of the mutations. This study is the first systematic ADPKD mutation analysis of both PKD1 and PKD2 genes in Chinese patients using denaturing high-performance liquid chromatography (DHPLC).

Methods: Both PKD1 and PKD2 genes were mutation screened in each proband from 65 families using DHPLC followed by DNA sequencing.

Novel variations found in the probands were checked in their family members available and 100 unrelated normal controls. Then the pathogenic potential of the variations of unknown significance was examined by evolutionary comparison, effects of amino acid substitutions on protein structure, and effects of splice site alterations using online mutation prediction resources.

Results: A total of 92 variations were identified, including 27 reported previously.

Definitely pathogenic mutations (ten frameshift, ten nonsense, two splicing defects and one duplication) were identified in 28 families, and probably pathogenic mutations were found in an additional six families, giving a total detection level of 52.3% (34/65). About 69% (20/29) of the mutations are first reported with a recurrent mutation rate of 31%.

Conclusions: Mutation study of PKD1 and PKD2 genes in Chinese Hans with ADPKD may contribute to a better understanding of the genetic diversity between different ethnic groups and enrich the mutation database.

Besides, evaluating the pathogenic potential of novel variations should also facilitate the clinical diagnosis and genetic counseling of the disease.

Author: Chaowen YuYuan YangLin ZouZhangxue HuJing LiYunqiang LiuYongxin MaMingyi MaDan SuSizhong Zhang
Credits/Source: BMC Medical Genetics 2011, 12:164

Relaxin improves poor blood flow and kidney function in a rat model of PKD

2011-12-09T05:49:00.000-05:00

Published on December 7, 2011 at 8:02 AM
Research presented at ASCB annual meeting
After a four-week course of the vasodilator hormone relaxin, kidney function and blood flow immediately improved in lab rats genetically altered to model polycystic kidney disease (PKD), a life-threatening genetic disorder, according to research presented on Dec. 6 at the American Society for Cell Biology Annual Meeting in Denver.

In addition to widening the blood vessels, relaxin lowered the collagen scores of the PKD rats, indicating that the drug had slowed scar formation or helped dissolve the old fibroid tissue that characterizes the kidneys of animals and humans with the disease, according to Heather Ward, Ph.D., and Angela Wandinger-Ness, Ph.D., of the University of New Mexico and collaborators.

PKD is a life-threatening genetic disorder that affects 600,000 Americans, according to the National Institute of Diabetes, Digestive, and Kidney Diseases (NIDDK). About 50% of individuals diagnosed with PKD develop end-stage renal disease by age 60.

The researchers also noted that in rats, relaxin reduced the size of the large fluid-filled cysts that gradually encroach on kidney function in human PKD patients.

PKD was the first disease to be recognized as a ciliopathy, a disorder characterized by defects in primary cilia, tiny hair-like structures that protrude from virtually every cell in the human body.

In the search of effective treatments, most PKD researchers have concentrated on halting or reversing PKD's characteristic cyst formation.
Read More: http://www.news-medical.net/news/20111207/Relaxin-improves-poor-blood-flow-and-kidney-function-in-a-rat-model-of-PKD.aspx?page=2

Just the facts about Polycystic Kidney Disease

2011-11-26T07:59:00.001-05:00

Just the facts about Polycystic Kidney Disease (PKD) - The most common life-threatening genetic disease in the world. It affects 600,000 Amercians and over 12.5 million people worldwide. Polycystic Kidney Disease (PKD) is more common than muscular distrophy, cystic fibrosis, down's syndrome, sickle cell anemia and hemophilia; combined. There is hope - Learn more at http://pkdcure.org/

Facts About Kidney Disease: Causes, Symptoms, and Diet

2011-11-21T05:49:00.000-05:00

(2011-11-16) The kidneys are required to help maintain fluid balance, but in the case of kidney damage fluids may need to be restricted. This article discusses why fluid assessment is an essential part of a kidney

Your kidneys play very important roles in body functions. Hence it is important to maintain a healthy kidney diet. Kidneys filter the blood and get rid of waste products of your body like uric acid from the breakdown of DNA, and urea from the metabolism of protein. At the same time they balance the levels of electrolyte in the body such as potassium and sodium, and also control blood pressure. Kidneys also supply the hormone called erythropoietin, which helps stimulate the bone marrow to produce red blood cells.
Sometimes no matter how careful you are with your kidneys, there are still chances that you will develop kidney problems. Here are some of the causes of kidney disease:
* High blood pressure – also known as hypertension, if uncontrolled, the kidneys will be damaged over time.
* Diabetes –type 1 and 2 diabetes can lead to a condition called diabetic nephropathy which is the major cause of kidney disease.
* Hereditary –if you have a family member who has a history of kidney disease then you are susceptible with the same disease. One example of this condition is the polycystic kidney disease wherein the two kidneys develop cysts.
* Glomerulonephritis –the inflammation or damage of the kidney’s filtration system. This condition if not treated immediately can cause kidney failure.
* Long term medications –some medications can be toxic to the tissues of the kidney which can lead to kidney failure over time.
* Other infections –include certain cancers, sickle cell disease, amyloidosis, heroine abuse, and HIV infection
If one of these conditions is present in your body then you are at a high risk of developing kidney disease. Your kidneys should be regularly monitored, but some changes can be made to lessen your chance of developing kidney failure treatment. It can include a change in lifestyle and diet. If you already have kidney disease, then you need to have constant medication, or a better natural option would be following a strict kidney diet. But how would you know if you already have a kidney disease? Here are the following symptoms you can take a look at:
* Swollen eyes, feet and hands (this condition is commonly known as edema)
* Loss of appetite
* Constant tiredness
* High blood pressure
* Constant feeling of thirst
* Shortness of breath
* Bad breath
* Weight loss
* Nausea and vomiting
* Constant itchiness of the skin
* Muscle cramps
* Tea-colored or cloudy urine
* A yellowish-brown trace on the skin
There are two types of kidney failure, chronic kidney failure or acute kidney failure. Both types can be life-threatening. In both circumstances, the kidneys stop functioning normally and cannot filter wastes or too much water from the blood. Due to this condition, toxic materials start to build up which can cause several complications that can affect different body systems. People who suffer from chronic kidney failure will need kidney transplant or dialysis to be able to survive. If you have kidney failure, or you know someone who has this disease, a strict kidney diet must be followed.
* Drink at least 8-10 glasses of water every day. The main function of your kidneys is to filter toxins from the blood and drain them off through urine. Without adequate amount of water, your kidneys can’t function very well. Generally, most chronic kidney disease and kidney stones are caused by inadequate water intake. You can also eat fruits and vegetables which contain 90 percent of water like cucumber, tomatoes, watermelon and zucchini.
* Eat more vegetables than meat. Too much protein intake can stress your kidneys.
* Avoid foods that have high levels of cholesterol. Eat nondairy products and lean meats instead. Also include whole grains in your kidney diet.
* Avoid goods that are heavily sweetened.
* Quit smoking. Smoking can increase blood pressure which is one of the major causes of kidney disease.
When planning a kidney diet it is still best to consult your physician or a dietician. The right kidney diet plan for you will also depend on the condition that you have. The key to a healthy kidney diet is dedication and the right people to back you up.

About The Publisher:
Kidney is one of the most important organs in our body, And having the right solution for the problem in one’s kidney is very hard to find due to different ideas about it. Kidney Diet have many ways in treating them and we just need to know and to perform them correctly. For more information visit my site at http://mykidneydiet.com/

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http://www.addpr.com/articles/health_fitness/95704.html

Critical evaluation of rituximab rescue in 27 patients with different types of kidney disease.

2011-10-19T05:57:00.000-04:00

Minerva Urol Nefrol. 2011 Dec;63(4):263-72.
Critical evaluation of rituximab rescue in 27 patients with different types of kidney disease.
Ganzemueller J, Hartmann B, Keller F, Stracke S.
SourceDepartment of Nephrology, School of Medicine, University of Ulm, Ulm, Germany - frieder.keller@uni-ulm.de.

Abstract
AIM: Rituximab is increasingly being used in the treatment of patients with kidney disease. We evaluated our clinical experience at the Ulm University Hospital.

METHODS: Since 2004, we have administered rituximab as rescue therapy to twenty-seven patients with kidney disease non-responsive to standard treatment. Indications for rituximab were progressive loss of kidney function in thirteen cases; nephrotic syndrome in five cases; humoral rejection after kidney transplantation in five cases and single cases of catastrophic antiphospholipid syndrome (CAPS), pre-emptive removal of ABO incompatible antibodies, pre-transplant removal of panel-reactive antibodies (PRA), and post-transplant lymphoproliferative disease (PTLD). Sixteen patients were treated with both, plasmapheresis and rituximab.

RESULTS: Kidney function recovered in five of thirteen cases. Nephrotic syndrome response was observed in two of five cases. In two of five patients with humoral rejection, kidney transplant function could be preserved. Antiphospholipid antibodies, blood group A antibodies and panel reactive antibodies successfully were reduced, and remission was achieved in the case of the patient with PTLD. Four patients died (15%). Adverse events (N.=10) and infectious complications (N.=15) were most likely due to immunosuppression in general and not to rituximab alone. Toxic leukoencephalopathy was a serious but reversible complication in three cases and occurred particularly after the administration of high-dose rituximab (>375 mg/m2).

CONCLUSION: Rituximab rescue was successful in 48% of our cases (13 of 27). Rituximab did not increase the complication risk of standard immunosuppression. But toxic leukoencephalopathy was identified as a significant rituximab complication.

PMID:21996981[PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/21996981

Excellent survival after liver transplantation for isolated polycystic liver disease: an European Liver Transplant Registry study.

2011-10-02T07:35:00.000-04:00

Transpl Int. 2011 Sep 29. doi: 10.1111/j.1432-2277.2011.01360.x. [Epub ahead of print]

Excellent survival after liver transplantation for isolated polycystic liver disease: an European Liver Transplant Registry study.
van Keimpema L, Nevens F, Adam R, Porte RJ, Fikatas P, Becker T, Kirkegaard P, Metselaar HJ, Drenth JP; for the European Liver and Intestine Transplant Association (ELITA).

Source Department of Gastroenterology and Hepatology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands Department of Hepatology, University Hospital KULeuven, Leuven, Belgium Centre Hépato-biliaire, AP-HP Hôpital Paul Brousse, Villejuif, France Department of Surgery, University Medical Center Groningen, Groningen, The Netherlands Department for General, Visceral and Transplant Surgery, Charite Campus Virchow, Universitätsmedizin Berlin, Berlin, Germany Department for General, Visceral and Transplant Surgery, Medizinische Hochschule Hannover, Hannover, Germany Department of Surgery and Transplantation, Rigshospitalet, University of Copenhagen, Denmark Department of Gastroenterology and Hepatology, Erasmus Medical Center, Rotterdam, The Netherlands.

Abstract
Patients with end-stage isolated polycystic liver disease (PCLD) suffer from incapacitating symptoms because of very large liver volumes. Liver transplantation (LT) is the only curative option. This study assesses the feasibility of LT in PCLD. We used the European Liver Transplant Registry (ELTR) database to extract demographics and outcomes of 58 PCLD patients. We used Kaplan-Meier survival analysis for survival rates. Severe abdominal pain (75%) was the most prominent symptom, while portal hypertension (35%) was the most common complication in PCLD. The explantation of the polycystic liver was extremely difficult in 38% of patients, because of presence of adhesions from prior therapy (17%). Karnofsky score following LT was 90%. The 1- and 5-year graft survival rate was 94.3% and 87.5%, while patient survival rate was 94.8% and 92.3%, respectively. Survival rates after LT for PCLD are good.

© 2011 The Authors. Transplant International © 2011 European Society for Organ Transplantation.

PMID:21955068[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21955068

Kidney disease marker predicts who will need dialysis

2011-09-27T05:17:00.000-04:00

September 09, 2011|By Shari Roan, Los Angeles Times / For the Booster Shots blogKidney disease affects about 20 million Americans, many of whom end up on dialysis. But there may be a way to identify and treat severe cases earlier in the course of the disease.

In a study published Friday, researchers said that measuring a hormone called FGF-23 can predict which patients will end up needing dialysis.

The hormone, fibroblast growth factor-23, was discovered fairly recently and has attracted a lot of attention from researchers for its crucial role in regulating phosphorus in the body. The new study showed that as kidneys fail, FGF-23 levels rise. Currently, doctors measure phosphorus levels to monitor patients with kidney disease. But FGF-32 appears to be more sensitive and begins to rise well before phosphorus changes are apparent.

"This discovery allows us to predict at-risk patients before they require dialysis," the lead investigator, Dr. Michel Chonchol, an associate professor of nephrology at the University of Colorado School of Medicine, said in a news release. "That's critical because approximately 23% of patients on dialysis die in the first year."

The study appears in the Journal of the American Society of Nephrology.

Return to Booster Shots blog.

Follow me: twitter.com/LATShariRoan
http://articles.latimes.com/2011/sep/09/news/la-heb-kidney-disease-20110909

Pharsight to Work with Critical Path Institute's Polycystic Kidney Disease Consortium on Disease Progression Modeling

2011-09-24T07:22:00.000-04:00

Consortium Includes Academic, Regulatory, and Industry Experts in Effort to Accelerate Pace of Medical Product Development
http://www.marketwatch.com/story/pharsight-to-work-with-critical-path-institutes-polycystic-kidney-disease-consortium-on-disease-progression-modeling-2011-09-07

ST. LOUIS, Sep 07, 2011 (BUSINESS WIRE) -- Pharsight, a market-leading provider of software and scientific consulting services to improve productivity and decision-making in clinical drug development, has announced they will be working with Critical Path Institute (C-Path)'s Polycystic Kidney Disease (PKD) Consortium to create and study quantitative models of disease progression in patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD).

The PKD Consortium is a successful collaboration between C-Path, the PKD Foundation, Clinical Data Interchange Standards Consortium (CDISC), and four leading academic medical centers (Tufts University, University of Colorado - Denver, Emory University, and Mayo Clinic). The Consortium is led by C-Path and funded through a grant from the PKD Foundation and philanthropic donations. Additionally, a representative from the U.S. Food and Drug Administration (FDA) serves as an active advisor to the Consortium.
"ADPKD is a debilitating genetic disease affecting more than 600,000 Americans and 12 million people worldwide for which there is currently no known cure or effective treatment," said Ronald Perrone, MD, Co-Director of the PKD Consortium and Professor of Medicine at Tufts University School of Medicine.
"This is a very exciting project that leverages the power of collaboration," said Eslie Dennis, MD, FCP, Executive Director of the PKD Consortium at C-Path. "Traditional endpoints of renal function only show changes very late in the course of the disease, making it difficult to assess the effectiveness of new medications. There is critical need for a biomarker that will assess disease progression at an earlier stage when patients may be more likely to respond to new therapies."

"We are very pleased about this significant scientific partnership with Pharsight," added Jill Panetta, PhD, Interim Chief Executive Officer for the PKD Foundation. "The PKD Consortium has brought together impressive resources in support of our mission to promote research that will lead to the discovery of treatments for PKD and improve the lives of all it affects."

The primary goals of the PKD Consortium are to develop CDISC research data standards for PKD and to use clinical data from PKD patients collected over many years through patient registries and clinical trials to support the FDA-qualification of an imaging biomarker, Total Kidney Volume (TKV), as an endpoint in drug development trials.

Scientists and physicians from Pharsight and the PKD Consortium will use the data collected to develop a quantitative disease progression model that will evaluate the relationship between TKV and the known complications of ADPKD, including rate of loss of kidney function, development of end-stage renal disease, and mortality. These analyses will be used to support the regulatory qualification of TKV as an accepted measure for assessing the progression of ADPKD in clinical trials in which new therapies are tested.

"Critical Path Institute is proud to be the facilitator of this ground breaking collaboration to accelerate the pace of drug development for this disease," said Raymond Woosley, MD, PhD, President and Chief Executive Officer of C-Path. "We welcome the opportunity to work with Pharsight and its team of scientists."

"Pharsight is honored to join this important and innovative project," added JF Marier, PhD, FCP, Vice President and Lead Scientist at Pharsight. "We are all committed to the development of a qualified measure that will encourage drug development organizations to test potential new disease-modifying treatments for ADPKD."

About Pharsight

Pharsight, a Certara(TM) company, is a market-leading provider of software products and scientific consulting services to help pharmaceutical and biotechnology companies improve their drug development process, regulatory compliance and strategic decision-making. Established in 1995, the company's goal is to help customers reduce the time, cost and risk of drug development. With more than 1200 customers worldwide, Pharsight products and services are used by all of the world's top 50 pharmaceutical firms. More information about Pharsight is available at http://www.pharsight.com/ .

About Critical Path Institute (C-Path)
An independent, non-profit organization established in 2005 with public and private philanthropic support from the Southern Arizona community, Science Foundation Arizona (SFAz), and the U.S. Food and Drug Administration (FDA), C-Path is committed to transformational improvement of the drug development process. An international leader in forming collaborations around this mission, C-Path has established first-of-its-kind global partnerships that currently include over 1,000 scientists from government, regulatory agencies, academia, patient advocacy organizations, and thirty major pharmaceutical companies. C-Path is headquartered in Tucson, Arizona, with offices in Phoenix, Arizona, and Rockville, Maryland. More information about C-Path is available at http://www.c-path.org/ .

About The PKD Foundation

Polycystic Kidney Disease affects one in 500 people, regardless of gender, age or ethnicity. More than 600,000 Americans and 12.5 million people worldwide suffer from this debilitating genetic disease. The PKD Foundation is the primary research, education and advocacy group working to find a treatment and a cure for Polycystic Kidney Disease. More information about PKD and the PKD Foundation is available at http://www.pkdcure.org/ .

Registered Trademarks and Trademarks

Pharsight is a registered trademark of Tripos, L.P. All other brands and product names are trademarks or registered trademarks of their respective holders.

SOURCE: Pharsight

Pharsight Contact:

Adam Rutkin, 408-737-6053

Director of Marketing and Business Development

arutkin@pharsight.com

or

Critical Path Institute Contact:

Lisa Romero, 520-547-3440

Communications and Strategic Outreach Manager

lromero@c-path.org

Scientists explore new model in battle against kidney disease

2011-09-08T08:22:00.000-04:00

September 8, 2011 — 6:31am ET | By Ryan McBride

A multi-organizational effort to combat polycystic kidney disease has turned to the scientists at software and consulting firm Pharsight to develop quantitative models of the disorder. It's another step in the Critical Path Institute's PKD Consortium quest to advance CDISC research data standards and an imaging biomarker for the kidney disease, which affects one in 500 Americans and more than 12 million people worldwide.

The group wants to develop the imaging biomarker, known as total kidney volume (TKV), and gain the FDA's support for the marker as a key measurement of autosomal dominant polycystic kidney disease in clinical trials for drugs against the genetic condition. Toward that end, Pharsight and the PKD Consortium aim to create a disease-progression model with data collected from studies of the ailment "that will evaluate the relationship between TKV and the known complications of ADPKD, including rate of loss of kidney function, development of end-stage renal disease and mortality," Pharsight said in a release.
"This is a very exciting project that leverages the power of collaboration," said Dr. Eslie Dennis, executive director of the PKD Consortium, in a statement. "Traditional endpoints of renal function only show changes very late in the course of the disease, making it difficult to assess the effectiveness of new medications. There is critical need for a biomarker that will assess disease progression at an earlier stage when patients may be more likely to respond to new therapies."

The groups involved in the consortium also include the PKD Foundation, a financial supporter of the effort, the Clinical Data Interchange Standards Consortium (CDISC), as well as experts from Emory University, the Mayo Clinic, Tufts University and the University of Colorado, Denver.

- here's the release

Read more: Scientists explore new model in battle against kidney disease - FierceBiotechIT http://www.fiercebiotechit.com/story/scientists-explore-new-model-battle-against-kidney-disease/2011-09-08#ixzz1XMYxHYTb

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Unhappy Camper: Boycott Peters Pond Park Sandwich MA

2011-08-24T11:40:00.000-04:00

Unhappy Camper: Boycott Peters Pond Park Sandwich MA

Heart Disease Prevalent in Children with Impaired Kidney Function

2011-08-19T04:41:00.000-04:00

Posted by Kristeen Moore on August 13, 2011 12:04 PM

Heart disease is more prevalent in children that have mild kidney problems, according to Science Daily. A study conducted by the Children’s Study of Philadelphia also found heart problems are responsible for 35 percent of deaths in young adults with poor kidney function.

586 children with chronic kidney problems were studied to help determine exactly how the kidneys play a role in the development of heart disease. According to Science Daily, an increase in blood pressure was found in children who had even mild kidney impairments. High blood pressure occurs when the force of blood flow against the blood vessels in above normal.

Metabolic problems, as well as delayed growth and puberty, were also found in the study participants.

"Our findings suggest that more aggressive interventions to improve blood pressure and metabolic abnormalities may be areas where interventions could slow chronic kidney disease progression and decrease the prevalence of cardiovascular disease in children and young adults with chronic kidney disease,” said Susan Furth, MD, as quoted by Science Daily.

There are a variety of causes of kidney dysfunction in children, from polycystic kidney disease to urinary tract problems. High blood pressure is common in children with kidney disease, so it is advisable that parents have their kids checked regularly. The National Kidney Foundation also recommends lifestyle changes, such as regular exercise, healthy diet and cutting down on salty foods.

http://www.thirdage.com/news/heart-disease-prevalent-in-children-with-impaired-kidney-function_08-13-2011

New medical FICO score sparks controversy, questions

2011-07-29T08:43:00.000-04:00

Jeremy M. Simon, On Thursday July 28, 2011, 8:00 am EDT

Within the next 12 months, whether you like it or not, about 10 million Americans are expected to be scored -- much like a credit score -- on how likely they are to fill a prescription and take all the pills the doctor ordered, on schedule.

FICO , creator of the widely used credit score that predicts whether you'll borrow responsibly, is now rolling out its new Medication Adherence Score.

FICO based its score on a formula that predicts whether you will take your prescription drugs. FICO says that since correct use of medication is important for patients, medical providers, insurers and pharmaceutical companies, the Medication Adherence Score will help achieve that goal. They predict it will improve therapy effectiveness and reduce health care costs.

The company says those who score low can be targeted for extra reminders and educational efforts, with the goal of making patients more likely to complete their prescribed regimens.

"It's very important to identify those people who may need that additional education and that additional help," says Dave Shellenberger, senior principal consultant in FICO's health care division.

Critics aren't so sure. Since the score uses information on patients' employment, homeownership and living situations, they say that in the current economic environment, the Medication Adherence Score may unfairly target people who have found themselves in challenging financial situations. It could also, they say, open the door for a new way for insurance companies to charge different prices for different scores. This happened in recent years to consumers buying auto insurance: The cost of those policies are now likely based on an auto insurance credit score .

What's in the score?
FICO launched the Medication Adherence Score on June 23, 2011. To create the scoring algorithm, FICO looked at data from a random sample of several million anonymous patients provided by a large pharmacy benefits manager. FICO observed patients who filled (or refilled) their prescriptions and patients who failed to, with the company then identifying those variables that best predicted medication adherence. For the Medication Adherence Score, those variables include age, gender, family size and asset information -- such as the likelihood of car ownership -- data also used by direct marketing companies. FICO says that with only a patient's name and address, it can pull the remainder of the necessary information from publicly available sources.

The scores range from 1 to 500. "The higher the score, the higher the likelihood a patient will be adherent to a drug regimen," FICO's Shellenberger says. FICO says patients who score 400 or higher are likely to take medication as prescribed, while those who score below 200 are at high risk of not taking medication. According to FICO, patients who earn a low score may receive a medication reminder in the form of an email, letter or phone call from their doctor -- tactics that would be too costly to apply across the board.

FICO says those who wouldn't want to receive notices should contact their health care providers and ask about their opt-out policies. High scorers who appear likely to take all their meds probably won't be contacted.

Click here to read the rest!

Conn. man finds kidney donor via Facebook‎

2011-07-28T12:30:00.000-04:00

STALLINGS, N.C. – For a decade now, David Ensely has lived with polycystic kidney disease. Doctors told him he needed a kidney to survive. He found one on Facebook.

"There's been times that I've been so sick I just wanted to die," Ensely said.

David’s sister, Jennifer Scoggins, set up a Facebook page to find her brother a kidney. She knew a positive outcome wasn't likely, but did it anyway after hearing it had worked for someone else.

"I just thought about it, 'Well, what do we have to lose?'” Scoggins said. “I mean, at this point, as sick as he was, why not?"

An old friend of David and Jennifer’s found the page on the social media site. He hadn’t spoken to either of them, besides on Facebook, for 15 years.

Single Gene Controls Growth of Polycystic Disease

2011-06-22T08:15:00.000-04:00

NEW HAVEN, Conn.—A single gene is central in the development of several forms of polycystic kidney and liver disease, Yale School of Medicine researchers reported in the June 19 issue of Nature Genetics.

The findings suggest manipulating activity of PKD1, the gene causing the most common form of polycystic kidney disease, may prove beneficial in reducing cysts in both liver and kidney.

"We found that these conditions are not the result of an all or nothing phenomenon," said Stefan Somlo, the C.N.H. Long Professor of Medicine and Genetics and Chief, Section of Nephrology and senior author of the study. "The less PKD1 is expressed, the more cysts develop. Conversely, expressing more PKD1 can slow the process."

The most common form of this condition is called autosomal dominant polycystic kidney disease (ADPKD), a condition passed on to children from one parent affected with the disease that is found in 600,000 people in the United States alone. Two genes, PKD1 and PKD2, are responsible for the onset of this condition.

PKD patients also develop cysts of the liver and Somlo and colleagues had previously identified families with identical cysts found only in the liver. They found two different genes were responsible for this related condition.

The researchers wanted to know how liver-only polycystic disease was related to ADPKD. In a series of experiments using both genetically engineered mouse models and biochemical studies, they found that the activity of only one of the four genes, PKD1, controlled cyst formation in the other forms of the disease. Experiments in mice showed that modulating dosage of PKD1 could slow disease progression.

"The data suggest the exciting possibility that targeting the activity of PKD1 may be beneficial for treatment of isolated polycystic liver disease, childhood recessive polycystic kidney disease and even a subset of adult ADPKD," said Somlo.
http://www.renalbusiness.com/news/2011/06/single-gene-controls-growth-of-polycystic-disease.aspx

Study say Aurora A may contribute to kidney disease

2011-06-18T06:51:00.000-04:00

by Kathy Jones on June 17, 2011 at 8:29 PM

A study in the June 13 issue of The Journal of Cell Biology says that the Aurora A kinase may contribute to polycystic kidney disease (PKD) by inactivating a key calcium channel in kidney cells.

Aurora A is an oncogene best known as a regulator of mitotic progression. But the kinase has important functions during interphase as well, when it can promote cilia disassembly and can be activated by elevated calcium levels. Because both calcium signaling and cilia are defective in PKD, researchers from the Fox Chase Cancer Center in Philadelphia wondered whether Aurora A might contribute to the pathology of this common genetic disease.

The researchers found that Aurora A was up-regulated and activated in epithelial cells lining the cysts in PKD patient kidneys. In addition, Aurora A bound to and phosphorylated a calcium channel called polycystin-2, whose gene, PKD2, is often mutated in autosomal dominant forms of PKD.

Polycystin-2 mediates the release of calcium from storage in the endoplasmic reticulum and calcium influx into cilia. Inhibition or knockdown of Aurora A boosted intracellular calcium levels, but this effect was less pronounced in kidney cells lacking polycystin-2, indicating that Aurora A normally lowers calcium levels by inactivating polycystin-2. Only small doses of inhibitor were required to increase calcium levels, suggesting that Aurora A may be a viable therapeutic target for boosting polycystin-2 activity in certain PKD patients. Senior author Erica Golemis now wants to investigate how Aurora A becomes up-regulated in PKD and whether inhibitors of the kinase can slow cyst formation in mouse models of the disease.

Read more: Study Says Aurora A May Contribute to Kidney Disease http://www.medindia.net/news/Study-Says-Aurora-A-May-Contribute-to-Kidney-Disease-86505-1.htm#ixzz1Pcih6P5M

Kidney stones

2011-06-13T06:52:00.000-04:00

Renal calculi; Nephrolithiasis; Stones - kidney
Last reviewed: January 14, 2009.

A kidney stone is a solid mass made up of tiny crystals. One or more stones can be in the kidney or ureter at the same time.

See also: Cystinuria

Causes, incidence, and risk factors
Kidney stones can form when urine contains too much of certain substances. These substances can create small crystals that become stones.

The biggest risk factor for kidney stones is dehydration.

Kidney stones may not produce symptoms until they begin to move down the tubes (ureters) through which urine empties into the bladder. When this happens, the stones can block the flow of urine out of the kidneys. This causes swelling of the kidney or kidneys, causing pain. The pain is usually severe.

Kidney stones are common. A person who has had kidney stones often gets them again in the future. Kidney stones often occur in premature infants.

Some types of stones tend to run in families. Certain kinds of stones can occur with bowel disease, ileal bypass for obesity, or renal tubule defects.

There are different types of kidney stones. The exact cause depends on the type of stone.

•Calcium stones are most common. They occur more often in men than in women, and usually appear between ages 20 - 30. They are likely to come back. Calcium can combine with other substances, such as oxalate (the most common substance), phosphate, or carbonate to form the stone. Oxalate is present in certain foods. Diseases of the small intestine increase the risk of forming calcium oxalate stones.

•Cystine stones can form in people who have cystinuria. This disorder runs in families and affects both men and women.

•Struvite stones are mostly found in women who have a urinary tract infection. These stones can grow very large and can block the kidney, ureter, or bladder.

•Uric acid stones are more common in men than in women. They can occur with gout or chemotherapy.

Other substances also can form stones.

Symptoms
The main symptom is severe pain that starts suddenly and may go away suddenly:

•Pain may be felt in the belly area or side of the back

•Pain may move to groin area (groin pain) or testicles (testicle pain)

Other symptoms can include:

•Abnormal urine color

•Blood in the urine

•Chills

•Fever

•Nausea

•Vomiting

Signs and tests
Pain can be severe enough to need narcotic pain relievers. The belly area (abdomen) or back might feel tender to the touch.

Tests for kidney stones include:

•Analysis of the stone to show what type of stone it is

•Uric acid level

•Urinalysis to see crystals and red blood cells in urine

Stones or a blockage of the ureter can be seen on:

•Abdominal CT scan

•Abdominal/kidney MRI

•Abdominal x-rays

•Intravenous pyelogram (IVP)

•Kidney ultrasound

•Retrograde pyelogram

Tests may show high levels of calcium, oxylate, or uric acid in the urine or blood.

Treatment
The goal of treatment is to relieve symptoms and prevent further symptoms. (Kidney stones that are small enough usually pass on their own.) Treatment varies depending on the type of stone and how severe the symptoms are. People with severe symptoms might need to be hospitalized.

When the stone passes, the urine should be strained and the stone saved and tested to determine the type.

Drink at least 6 - 8 glasses of water per day to produce a large amount of urine. Some people might need to get fluids through a vein (intravenous).

Pain relievers can help control the pain of passing the stones (renal colic). For severe pain, you may need to take narcotic pain killers or nonsteroidal anti-inflammatory drugs (NSAIDS) such as ibuprofen.

Depending on the type of stone, your doctor may prescribe medicine to decrease stone formation or help break down and remove the material that is causing the stone. Medications can include:

•Allopurinol (for uric acid stones)

•Antibiotics (for struvite stones)

•Diuretics

•Phosphate solutions

•Sodium bicarbonate or sodium citrate (which make the urine more alkaline)

Surgery is usually needed if:

•The stone is too large to pass on its own

•The stone is growing

•The stone is blocking urine flow and causing an infection or kidney damage

Today, most treatments are much less invasive than in the past.

•Extracorporeal shock-wave lithotripsy is used to remove stones slightly smaller than a half an inch that are located near the kidney. This method uses ultrasonic waves or shock waves to break up stones. Then, the stones leave the body in the urine.

•Percutaneous nephrolithotomy is used for large stones in or near the kidney, or when the kidneys or surrounding areas are incorrectly formed. The stone is removed with an endoscope that is inserted into the kidney through a small opening.

•Ureteroscopy may be used for stones in the lower urinary tract.

•Standard open surgery (nephrolithotomy) may be needed if other methods do not work or are not possible.

Expectations (prognosis)
Kidney stones are painful but usually can be removed from the body without causing permanent damage. They tend to return, especially if the cause is not found and treated.

Complications
•Decrease or loss of function in the affected kidney

•Kidney damage, scarring

•Obstruction of the ureter (acute unilateral obstructive uropathy)

•Recurrence of stones

•Urinary tract infection

Calling your health care provider
Call your health care provider if you have symptoms of a kidney stone.

Also call if symptoms return, urination becomes painful, urine output decreases, or other new symptoms develop.

Prevention
If you have a history of stones, drink plenty of fluids (6 - 8 glasses of water per day) to produce enough urine. Depending on the type of stone, you might need to take medications or other measures to prevent the stones from returning.

You may need to change your diet to prevent some types of stones from coming back.

References
1.Cameron MA, Sakhaee K. Uric acid nephrolithiasis. Urol Clin North Am. 2007;34(3):335-346. [PubMed: 17678984]
2.Chandhoke PS. Evaluation of the recurrent stone former. Urol Clin North Am. 2007; 34(3):315-322. [PubMed: 17678982]
3.Finkielstein VA. Strategies for preventing calcium oxalate stones. CMAJ. 2006;174(10):1407-1409. [PubMed: 16682705]
4.Pietrow PK, Preminger GM. Evaluation and medical management of urinary lithiasis. In: Wein AJ, ed. Campbell-Walsh Urology. 9th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 43.
Review Date: 1/14/2009.

Reviewed by: Louis S. Liou, MD, PhD, Assistant Professor of Urology, Department of Surgery, Boston University School of Medicine. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001493/

Adult polycystic kidney disease management

2011-06-13T06:49:00.000-04:00

Christopher M. Moon, Laura Gunder, DHSc, MHE, PA-C, and Ami R. Steele, MMSc, PA-C
June 06 2011
At a glance
■Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited cause of chronic kidney disease.
■Patients may present with flank or abdominal pain, cystitis secondary to UTI, hematuria and headaches.
■There is no proven treatment available that will prevent or delay the progression of ADPKD.
■About 50% of ADPKD patients will require a dialysis or a renal transplant by the age of 60 years.
Autosomal dominant polycystic kidney disease (ADPKD), also referred to as adult PKD, is the most common genetic cause of chronic renal disease.1 Among all hereditary diseases, ADPKD is 20 times more common than Huntington's chorea, 15 times more common than cystic fibrosis, and 10 times more common than sickle cell disease.2 As research continues, the understanding of the mechanisms of the disease has led to an increase in clinical trials available to patients. Many of these trials show promise in preventing cyst formation, which is the underlying cause of renal failure attributable to ADPKD.
A comprehensive understanding of the disease process will enable providers to accurately diagnose and manage patients with this condition. While there is currently no approved cure for the disease,3 it is crucial for clinicians to update their knowledge on the topic as new information is discovered and new treatments are made available. It is the role of the primary-care provider to manage patients' overall health and offer prompt treatment of complications as well as referral to a nephrologist when appropriate.   

Prevalence and epidemiology 
ADPKD has an estimated prevalence of one case in every 500 people, affecting approximately 600,000 Americans and as many as four to six million people worldwide.4 As the most common inherited disorder of the kidneys in humans, ADPKD afflicts approximately 10% of the patient population with end stage renal disease (ESRD).2 

ADPKD is considered a systemic disorder and results from mutations in either the PKD1 or PKD2 gene.5 The PKD1 gene is found on the short arm of chromosome 16, while the PKD2 gene is found on chromosome 4. The prevalence is 85%-90% having the PKD1 mutation, with the remaining 10%-15% having the PKD2 mutation.6  

The PKD1 gene encodes for polcystin-1, a large receptor-like molecule. The PKD2 gene encodes for polycytin-2, which acts like an ion channel protein. Both polcystin-1 and 2 are transmembrane proteins that are present in all segments of nephrin, a protein necessary for proper function of the renal filtration barrier, and are involved with the slit diaphragm. It is not certain whether the proteins act together or independently to carry out their functions. They are thought to regulate epithelial cell gene transcription, differentiation, apoptosis, and cell matrix interactions. Improper functioning of these proteins leads to epithelial differentiation, uncontrolled proliferation, apoptosis, altered cell polarity, disorganized surrounding extracellular fluid, increased fluid sections, and the abnormal expression of several genes. Cyclic adenosine monophosphate levels increase and are thought to be secondary to vasopressin stimulation. This may lead to cystogenesis by causing an increase in cell proliferation and fluid secretion into the cyst through aquaporin channels and chloride channels.5 When cysts enlarge, they begin to compress adjacent parenchyma, causing ischemia and occluding normal tubules. This leads to progressive impairment of renal function.7  

Patient presentation and history 
The initial workup of a patient presenting with ADPKD should include a full history and physical exam. On physical exam, large kidneys may be a palpable sign, but most patients will present with one or more of the following signs and symptoms:6,7 

Pain—Flank or abdominal pain secondary to mass effect, infection, bleeding into the cyst, and nephrolithiasis is common. 

Chills and fever may accompany an infection. 

Hematuria—Cystic ruptures into the renal pelvis may result in gross hematuria. Kidney stones and urinary tract infections (UTIs) can also cause gross hematuria. Gross hematuria should be closely monitored and should last no longer than seven days. 

Nephrolithiasis—Kidney stones, most of which are composed of calcium oxalate, are prevalent in up to 20% of patients with PKD. 

Hypertension—Almost all patients will develop hypertension during the course of the disease, with nearly half being hypertensive at the time of presentation. Activation of the renin-angiotensin-aldosterone system (RAAS) due to cyst-induced ischemia seems to be the cause. 

Cerebral aneurysms—Arterial aneurysms within the circle of Willis (circulus arteriosus cerebri) occur in about 10%-15% of patients with PKD and can be a source of headaches. 

Blood-vessel abnormalities—Mitral valve prolapse, aortic aneurysms, and aortic valve abnormalities 

Colonic diverticulitis with left-lower-quadrant pain 

Ophthalmic exam may reveal arteriovenous nicking and papilledema (optic disc swelling secondary to elevated intracranial pressure). 

ESRD signs and symptoms in late stage of disease—Malaise, cardiac arrhythmias, hypertension, anemia, fatigue, edema, and tetany.  

ADPKD workup 
In the initial workup of an individual with ADPKD, special attention should be given to the family history, social history, and medical history as well as to the genitourinary, GI, and cardiac/vascular portions of the physical exam. Pertinent family history findings include first-degree relatives with ADPKD or ESRD, stroke, intracranial aneurysms, heart-valve disorders, and colonic diverticulitis. The patient may present with flank or abdominal pain, hematuria, cystitis secondary to UTI, and headaches. Physical findings may include palpable kidneys and/or hepatomegaly. Hypertension is often the first detectable abnormality, but the patient may also have symptoms of renal insufficiency. Be alert for hernia-repair scars in the inguinal or umbilical regions. A cardiac murmur may also be noted during the cardiac exam.  

Once family history or exam findings have raised suspicion of ADPKD, laboratory studies (comprehensive metabolic profile, urinalysis [UA], fasting lipid panel, complete blood count, and possibly a parathyroid hormone level) and imaging studies should follow.  

Creatinine is used to calculate the glomerular filtration rate (GFR), which allows for staging of the disease. The staging of renal failure is as follows:  

Stage 1 - GFR >90 mL/min/1.73 m2 

Stage 2 - GFR 60-90  

Stage 3 - GFR 30-60  

Stage 4 - GFR 15-30 

Stage 5 - GFR<15  

CLICK HERE FOR TABLE

Pertinent findings on UA include microalbuminuria and hematuria—both of which may indicate renal dysfunction—and leukocyturia, which may signify a UTI.   The most common initial imaging study for suspected PKD is an abdominal ultrasound, which is cost-effective and safe for the patient. The Ravine criteria are used as a standard when interpreting ultrasound results for the diagnosis of ADPKD.8 These criteria are based on the patient's age, family history, and number of cysts (Table 1).   Sonographic diagnostic criteria for patients at 50% risk for ADPKD include at least two unilateral or bilateral cysts in people younger than age 30 years; two cysts in each kidney in patients aged 30-59 years; and four cysts in each kidney in patients older than age 60 years. Sensitivity of these criteria is nearly 100% for patients aged 30 years or older and for younger patients with PKD1 mutations but only 67% for patients younger than age 30 years with PKD2 mutations. Therefore, CT scan or MRI should be used in this group. In a child at 50% risk for ADPKD, large echogenic kidneys (without distinct macroscopic cysts) are diagnostic.9  Extrarenal findings may include hepatic and pancreatic cysts. If the results of the ultrasound are inconclusive, CT or MRI may be beneficial, as these imaging studies are more sensitive than ultrasound for detecting cysts. MRI may also be used to diagnose intracranial aneurysms if patients have headaches or a family history of stroke. Optional procedures include barium enema to diagnose diverticuli and an echocardiography to evaluate for valvular abnormalities.10,11   Genetic testing can be with a 95% accuracy of diagnosis: (1) when imaging results are equivocal or inconclusive; (2) to confirm a presumed diagnosis in the absence of family history of ADPKD (conclusive diagnosis in these patients relies on mutation analysis); and (3) when a definite diagnosis is required in a younger patient (e.g., a potential living related kidney donor).11    Treatment options   No proven treatment available will prevent or delay the progression of ADPKD. Treatment options are mostly supportive and preventive with the goal of slowing the progression of renal failure, managing complications, and prolonging life.11 Some promising trials are under way for new medications that may slow the rate of cyst formation, but the results will not be known for several years.   The targeted complications to be considered include:  Lifestyle changes. Diet modification should include protein restriction, lowered salt intake, decreased caffeine intake, and increased daily water intake. One study in progress is designed to determine the effects of increased water intake in amounts greater than three liters per day.12 The increased water intake is suspected to suppress vasopressin, which is thought to play a role in cyst formation. Patients who consume such large volumes of water are at heightened risk for hyponatremia, so sodium levels should be monitored regularly.10,13  Hypertension. Tight control of BP is thought to delay or prevent progression of the disease. Increased BP is considered attributable to an activation of the RAAS, so blockage of this system is the focus of treatment. Although no guidelines have been set for ADPKD, most clinicians agree to follow the recommendation from the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure of a BP <130/90 mm Hg. Studies are under way to determine whether even lower BP levels are beneficial. ACE inhibitors are considered first-line treatment followed by angiotensin II receptor blockers (ARBs) and direct renin inhibitors. Patients taking ACE inhibitors must have their creatinine and potassium monitored routinely for increased levels. Alternate treatment options include calcium channel blockers, beta blockers, and/or diuretics.8,11,13   UTIs. Increased frequency of UTIs is correlated with poorer outcomes in patients with PKD. Patient education and prompt treatment is crucial. Complications of UTI include obstruction and migration of infection to include the kidney, which can be devastating. Treatment can be started empirically with an antibiotic, but a specimen should be sent for culture and sensitivity so that proper therapy can be provided.8,11,13  Hyperlipidemia. Because elevated lipid levels have a coronary heart disease risk equivalent in patients with PKD, aggressive treatment should be implemented as needed. Statins are the first treatment option for lowering LDL and raising HDL. Statins may help preserve renal function, but this has not been proven.8,11,13   Pain. Pain can be caused by compression associated with enlarged kidneys, renal infections, cyst rupture, kidney stones, and even renal tumors. Most sources are self-limiting and can be controlled with rest and either acetaminophen, nonsteroidal anti-inflammatory drugs, or opioid analgesics. Treatment options for enlarged cysts include aspiration, sclerotic injections, or laparoscopic/surgical cyst fenestration.8,11,13   Nephrolithiasis. There are several ways to manage renal stones. For small stones, pain management with conservative observation may be indicated. Potassium citrate is indicated for three types of stones seen in ADPKD: (1) uric acid stones; (2) hypocitraturic calcium oxalate nephrolithiasis; and (3) distal acidification defects.11 For stones that do not spontaneously pass, urology referral is indicated. At this point, lithotripsy, percutaneous nephrolithotomy, and retrograde retrieval of stones are viable treatment options.8,11,13  Extrarenal complications. Intracranial aneurysms should be managed by a neurologist. Clipping or coiling are options for aneurysms >8 mm. Monitor heart-valve disorders with echocardiography, which can be used to assess the severity of need for valve-replacement surgery.8,11,13 

Renal failure. A patient progressing into Stage 4 of renal failure should prepare for kidney replacement. Renal transplant is the treatment of choice. Look within the family for possible donors, and place the patient on the donor waiting list. Dialysis is a second-line option for a patient on the donor waiting list or a candidate suitable for replacement. Access for dialysis may be through a vascular site, including a catheter, graft, or fistula. Another viable option is peritoneal dialysis.8,11,13  

Medications under trial. Several trials are examining treatments for ADPKD. The more promising include the vasopressin receptor antagonist tolvaptan, the somatostatin inhibitor octreotide, the kinase inhibitor everolimus, epidermal growth factor receptor inhibitors, tyrosine kinase, Src kinase, roscovitine, and ACE inhibitor/ARB antagonist combinations.8,11,13 For more information of ongoing clinical trials, visit ClinicalTrials.gov.  

Prognosis  
Approximately 50% of ADPKD patients will develop ESRD and require either a renal transplant or dialysis by age 60 years. The major factor for prognosis is the form of gene mutation present in the patient. Although the two forms of ADPKD (ADPKD1 and 2) share similar clinical features, renal prognosis is vastly different. Studies show that ADPKD2 is a milder disease, based on the age of onset of ESRD. The median age of renal survival for those with this form of ADPKD is 68 years. For those with ADPKD1, the median age of renal survival is 53 years.6 

Other factors that can improve outcomes are tight control of BP, adherence to dietary recommendations, and prevention/prompt treatment of UTIs.5,6   

Conclusion 
The understanding of ADPKD has improved over the past decade. A comprehensive approach to caring for people with this disease that includes early detection, management of symptoms, and referral to a nephrologist when appropriate is imperative.

Mr. Moon is a second-year student in the physician assistant program at the Medical College of Georgia in Augusta, where Dr. Gunder is assistant professor and director of research and faculty development, and Ms. Steele is assistant professor. 

References 
1. Torres VE, Harris PC. Autosomal dominant polycystic kidney disease: the last 3 years. Kidney Int. 2009;76:149-168.

2. Ross JE. Diseases of the kidney. In: AK David, DM Phillips, JE Scherger, TA Johnson, eds. Family Medicine: Principles and Practice, 6th ed. New York: Springer-Verlag New York, Inc.; 2003:838. 

3. Patel V, Chowdhury R, Igarashi P. Advances in the pathogenesis and treatment of polycystic kidney disease. Curr Opin Nephrol Hypertens. 2009;18:99-106. 

4. Gunder LM, Martin SA. Essentials of Medical Genetics for Health Professionals. Sudbury, Mass.: Jones & Bartlett Learning; 2011:155. 

5. Salant DJ, Patel PS. Polycystic kidney disease and other inherited tubular disorders. In: Kasper DL, Braunwald E, Fauci AS, et al., eds. Harrison's Principles of Internal Medicine. 17th ed. New York, N.Y.: The McGraw-Hill Companies; 2008:1797-1805. 

6. Watnick S, Morrison G. Cystic diseases of the kidney. In: McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis & Treatment. 49th ed. New York, N.Y.: McGraw-Hill; 2010:846-848. 

7. Mcaninch JW. Adult polycystic kidney disease. In: Tanagho EA, McAninch JW, eds. Smith's GeneralUrology. 17th ed. Columbus, Ohio: McGraw-Hill;2008:507-512. 

8. Braun WE. Autosomal dominant polycystic kidney disease: emerging concepts of pathogenesis and new treatments. Cleve Clin J Med. 2009;76:97-104.

9. Ravine D, Gibson RN, Walker RG, et al. Evaluation of ultrasonographic diagnostic criteria for autosomal dominant polycystic kidney disease 1. Lancet. 1994;343:824-827. 

10. eMedicine. Polycystic kidney disease.

11. Epocrates Online. Polycystic kidney disease.

12. Grantham JJ. Therapy for polycystic kidney disease? It's water,  stupid! J Am Soc Nephrol. 2008;19:1-7.

13. UpToDate. Course and treatment of autosomal dominant polycystic kidney disease.

 All electronic documents accessed May 15, 2011. 
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Smilage Dental: Dr Fred Attarzadeh of Smilage Dental Franklin and Framingham MA

2011-05-09T18:38:00.000-04:00

Smilage Dental: Dr Fred Attarzadeh of Smilage Dental Franklin and Framingham MA

UCSB Scientists Discover New Drug Target for Kidney Disease

2011-05-09T06:44:00.000-04:00

PRESS RELEASE

UCSB Scientists Discover New Drug Target for Kidney Disease
April 26, 2011

(Santa Barbara, Calif.) –– Two discoveries at UC Santa Barbara point to potential new drug therapies for patients with kidney disease. The findings are published in this week's issue of the Proceedings of the National Academy of Sciences.

Over 600,000 people in the U.S., and 12 million worldwide, are affected by the inherited kidney disease known as autosomal-dominant polycystic kidney disease, or ADPKD. The disease is characterized by the proliferation of cysts that eventually debilitate the kidneys, causing kidney failure in half of all patients by the time they reach age 50.

Currently, no treatment exists to prevent or slow cyst formation, and most ADPKD patients require kidney transplants or lifelong dialysis for survival, explained Thomas Weimbs, director of the laboratory where the discoveries were made. Weimbs is an associate professor in the Department of Molecular, Cellular and Developmental Biology and the Neuroscience Research Institute at UCSB.

First, Weimbs and his research team discovered a molecular mechanism that sheds light on the disease. The mechanism concerns polycystin-1, a protein that is mutated in ADPKD patients. The team discovered how this protein regulates a well-known transcription factor called STAT3. Transcription factors transcribe information from DNA to RNA, from specific genes. Second, the team discovered that STAT3 is strongly, and aberrantly, activated in polycystic kidneys.

"The clinical significance of these discoveries lies in the fact that STAT3 is also known to be aberrantly activated in many forms of cancer and is considered an important drug target for cancer therapy," said Weimbs. "Numerous STAT3 inhibitors are currently being developed and tested, and several experimental drugs are already available. Our results suggest that STAT3 activation is a driving force for the cyst growth that leads to polycystic kidneys in ADPKD. Therefore, STAT3 may be a highly promising drug target for the treatment of ADPKD."
Weimbs explained further that STAT3 is a signaling molecule that is activated in response to many different growth factors binding to specific receptors on the surface of kidney cells. In response to these growth factors hitting the cell, STAT3 is activated. That causes STAT3 to turn on the expression of certain genes. This activity causes the cells to proliferate, as they do in cancer.

"In polycystic kidney disease, we have strong proliferation, but it is similar to having benign tumors –– where the tumor stays in place," said Weimbs. "The cysts keep growing, but they do not metastasize or invade other tissues as do cancerous tumors. Polycystic kidneys are full of small, benign tumors or cysts. This is still very destructive, because eventually the disease will destroy the kidney."

The research team is currently testing STAT3 as a drug target in mice with ADPKD.

The first author of the paper is Jeffrey J. Talbot, a postdoctoral fellow in the Weimbs lab. The other co-authors from UCSB are Jonathan M. Shillingford, Shivakumar Vasanth, Nicholas Doerr, and Sambuddho Mukherjee. Additional co-authors are Terry Watnick, Johns Hopkins University School of Medicine; and Mike Kinter, Oklahoma Medical Research Foundation. The National Institutes of Health funded the research.

http://www.ia.ucsb.edu/pa/display.aspx?pkey=2475

Systems biology approach to identify transcriptome reprogramming and microRNA targets during the progression of Polycystic Kidney Disease

2011-04-26T07:55:00.000-04:00

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by cyst formation throughout the kidney parenchyma. It is caused by mutations in either of two genes, PKD1 and PKD2.

Mice that lack functional Pkd1 (Pkd1-/-), develop rapidly progressive cystic disease during embryogenesis, and serve as a model to study human ADPKD. Genome wide transcriptome reprogramming and the possible roles of micro-RNAs (miRNAs) that affect the initiation and progression of cyst formation in the Pkd1-/- have yet to be studied.

miRNAs are small, regulatory non-coding RNAs, implicated in a wide spectrum of biological processes. Their expression levels are altered in several diseases including kidney cancer, diabetic nephropathy and PKD.

Results: We examined the molecular pathways that modulate renal cyst formation and growth in the Pkd1-/- model by performing global gene-expression proling in embryonic kidneys at days 14.5 and 17.5

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Identification Of New Role For Cilia Protein In Mitosis

2011-04-24T09:07:00.000-04:00

Researchers at the University of Massachusetts Medical School have described a previously unknown role for the cilia protein IFT88 in mitosis, the process by which a dividing cell separates its chromosomes containing the cell's DNA into two identical sets of new daughter cells. Published in advance online by Nature Cell Biology, this newly discovered function for IFT88 suggests a possible alternative or contributory cause for cilia-related diseases such as primary ciliary dyskinesia, and polycystic kidney disease.

Famous for its ability to build cilia, a slender protrusion responsible for motility and sensory input, IFT88 is part of a family of transport proteins and cellular machinery that is responsible for moving materials from the cell body to the cilia. These cellular materials are necessary for the proper formation and maintenance of cilia and in the absence of IFT88 cilia are either unable to form or are defective. Over the last several years, scientists have linked cilia dysfunction to a number of diseases now known as ciliopathies. In particular, the loss of IFT88, one of the best-studied cilia proteins, has been associated with polycystic kidney disease (PKD). PKD is characterized by the presence of multiple cysts in the kidneys and is believed to be caused by cilia dysfunction in kidney cells.
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Sirolimus

2011-04-03T18:29:00.000-04:00

Sirolimus(sir oh' li mus)
Last Revision: February 10, 2010.

WarningSirolimus may increase the risk that you will develop an infection or cancer, especially lymphoma (cancer of a part of the immune system) or skin cancer. To reduce your risk of skin cancer, plan to avoid unnecessary or prolonged exposure to sunlight and to wear protective clothing, sunglasses, and sunscreen during your treatment. If you experience any of the following symptoms, call your doctor immediately: fever, sore throat, chills, frequent or painful urination, or other signs of infection; new sores or changes on the skin; night sweats; swollen glands in the neck, armpits, or groin; unexplained weight loss; trouble breathing; chest pain; weakness or tiredness that does not go away; or pain, swelling, or fullness in the stomach.

Sirolimus may cause serious side effects or death in patients who have had liver or lung transplants. This medication should not be given to prevent rejection of liver or lung transplants.

Keep all appointments with your doctor and the laboratory. Your doctor will order certain tests to check your body's response to sirolimus.

Talk to your doctor about the risks of taking sirolimus.

Why is this medication prescribed?
Sirolimus is used in combination with other medications to prevent rejection of kidney transplants. Sirolimus is in a class of medications called immunosuppressants. It works by suppressing the body's immune system.

How should this medicine be used?
Sirolimus comes as a tablet and a solution (liquid) to take by mouth. It is usually taken once a day, either always with food or always without food. To help you remember to take sirolimus, take it around the same time every day. Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take sirolimus exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor.

Swallow the tablets whole; do not split, chew, or crush them.

Your doctor will probably adjust your dose of sirolimus during your treatment, usually not more than once every 7 to 14 days.

Continue to take sirolimus even if you feel well. Do not stop taking sirolimus without talking to your doctor.

Sirolimus solution may develop a haze when refrigerated. If this happens, let the bottle stand at room temperature and gently shake it until the haze goes away. The haze does not mean that the medication is damaged or unsafe to use.

To use the bottles of solution, follow these steps:

•Open the solution bottle. On first use, insert the plastic tube with stopper tightly into the bottle until it is even with the top of the bottle. Do not remove from the bottle once inserted.

•For each use, tightly insert one of the amber syringes, with the plunger fully pushed in, into the opening in the plastic tube.

•Draw up the amount of solution your doctor has prescribed by gently pulling out the plunger of the syringe until the bottom of the black line of the plunger is even with the correct mark on the syringe. Keep the bottle upright. If bubbles form in the syringe, empty the syringe into the bottle and repeat this step.

•Empty the syringe into a glass or plastic cup containing at least 2 ounces (60 milliliters [1/4 cup]) of water or orange juice. Do not use apple juice, grapefruit juice, or other liquids. Stir vigorously for 1 minute and drink immediately.

•Refill the cup with at least 4 ounces (120 milliliters [1/2 cup]) of water or orange juice. Stir vigorously and drink the rinse solution.

•Throw away the used syringe.

If you need to carry a filled syringe with you, snap a cap onto the syringe and put the syringe in the carrying case. Use the medication in the syringe within 24 hours.

Other uses for this medicine
Sirolimus also is used sometimes to treat psoriasis. Talk to your doctor about the possible risks of using this medication for your condition.

This medication may be prescribed for other uses; ask your doctor or pharmacist for more information.

What special precautions should I follow?
Before taking sirolimus,

•tell your doctor and pharmacist if you are allergic to sirolimus, any other medications, or any of the ingredients in sirolimus tablets or solution. Ask your pharmacist for a list of the ingredients.

•tell your doctor and pharmacist what prescription and nonprescription medications, vitamins, and nutritional supplements you are taking. Be sure to mention any of the following: aminoglycoside antibiotics such as amikacin, gentamicin, kanamycin, neomycin (Neo-Fradin, Neo-Rx), streptomycin, and tobramycin (Tobi); amphotericin B (Abelcet, AmBisome, Amphocin, Fungizone); angiotensin-converting enzyme (ACE) inhibitors such as benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec), fosinopril (Monopril), lisinopril (Prinivil, Zestril), moexipril (Univasc), perindopril (Aceon), quinapril (Accupril), ramipril (Altace), and trandolapril (Mavik); antifungals such as clotrimazole (Lotrimin), fluconazole (Diflucan), itraconazole (Sporanox), ketoconazole (Nizoral), and voriconazole (Vfend); bromocriptine (Cycloset, Parlodel); cimetidine (Tagamet); cisapride (Propulsid) (not available in the U.S.); clarithromycin (Biaxin); danazol (Danocrine); diltiazem (Cardizem, Dilacor, Tiazac); erythromycin (E.E.S., E-Mycin, Erythrocin); HIV protease inhibitors such as indinavir (Crixivan) and ritonavir (Norvir, in Kaletra); certain medications for cholesterol; medications for seizures such as carbamazepine (Tegretol), phenobarbital (Luminal), and phenytoin (Dilantin); metoclopramide (Reglan); nicardipine (Cardene); rifabutin (Mycobutin); rifampin (Rifadin, Rimactane); rifapentine (Priftin); telithromycin (Ketek); troleandomycin (TAO) (not available in the U.S.); and verapamil (Calan, Covera, Isoptin, Verelan). Your doctor may need to change the doses of your medications or monitor you carefully for side effects.

•if you are taking cyclosporine (Neoral) soft gelatin capsules or solution, take them 4 hours before sirolimus.

•tell your doctor what herbal products you are taking, especially St. John's wort.

•tell your doctor if you have or have ever had high cholesterol or triglycerides or liver disease.

•tell your doctor if you are pregnant, plan to become pregnant, or are breast-feeding. You should use an effective method of birth control before starting to take sirolimus, while taking sirolimus, and for 12 weeks after stopping sirolimus. If you become pregnant while taking sirolimus, call your doctor.

•if you are having surgery, including dental surgery, tell the doctor or dentist that you are taking sirolimus.

•do not have any vaccinations without talking to your doctor.

What special dietary instructions should I follow?
Avoid drinking grapefruit juice while taking this medication.

What should I do if I forget a dose?
Take the missed dose as soon as you remember it. However, if it is almost time for the next dose, skip the missed dose and continue your regular dosing schedule. Do not take a double dose to make up for a missed one.

What side effects can this medication cause?
Sirolimus may cause side effects. Tell your doctor if any of these symptoms are severe or do not go away:

•stomach pain

•headache

•constipation

•diarrhea

•nausea

•joint pain

Some side effects can be serious. The following symptoms are uncommon, but if you experience any of them or those listed in the IMPORTANT WARNING section, call your doctor immediately:

•unusual bleeding or bruising

•cough

•swollen, red, cracked, scaly skin

•hives

•rash

•itching

•difficulty breathing or swallowing

•swelling of the face, throat, tongue, lips, eyes, hands, feet, ankles, or lower legs

•hoarseness

Sirolimus may cause other side effects. Call your doctor if you have any unusual problems while taking this medication.

If you experience a serious side effect, you or your doctor may send a report to the Food and Drug Administration's (FDA) MedWatch Adverse Event Reporting program online [at http://www.fda.gov/Safety/MedWatch] or by phone [1-800-332-1088].

What storage conditions are needed for this medicine?
Keep this medication in the container it came in, tightly closed, and out of reach of children. Store tablets at room temperature and away from light, excess heat, and moisture (not in the bathroom). Keep liquid medication in the refrigerator, away from light, closed tightly, and throw away any unused medication one month after the bottle is opened. Do not freeze. If needed, you may store the bottles for up to 15 days at room temperature. Throw away any medication that is outdated or no longer needed. Talk to your pharmacist about the proper disposal of your medication.

In case of emergency/overdose
In case of overdose, call your local poison control center at 1-800-222-1222. If the victim has collapsed or is not breathing, call local emergency services at 911.

What other information should I know?
Do not let anyone else take your medication. Ask your pharmacist any questions you have about refilling your prescription.

It is important for you to keep a written list of all of the prescription and nonprescription (over-the-counter) medicines you are taking, as well as any products such as vitamins, minerals, or other dietary supplements. You should bring this list with you each time you visit a doctor or if you are admitted to a hospital. It is also important information to carry with you in case of emergencies.

Other names
•Rapamycin

American Society of Health-System Pharmacists, Disclaimer

AHFS® Consumer Medication Information. © Copyright, 2011. The American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland. All Rights Reserved. Duplication for commercial use must be authorized by ASHP.

The following brand names are from RxNorm, a standardized nomenclature for clinical drugs produced by the National Library of Medicine:
Brand names
•Rapamune

Organizations Related to Donation & Transplantation

2011-03-27T06:45:00.000-04:00

Organ Donation and Transplantation Save Lives

Organ donation begins with a person who recognizes an opportunity to help others, enrolls in a state donor registry, and shares the decision to be a donor with family members and friends. The culmination of the process occurs when the person donates - and saves or enhances the lives of as many as eight people who need an organ transplant. In the United States, the Health Resources and Services Administration of the U. S. Department of Health and Human Services has oversight of the Organ Procurement and Transplantation Network (OPTN).

American Board of Transplant Coordinators

American Foundation for Donation and Transplantation
American Society of Nephrology
American Society of Transplant Surgeons
American Society of Transplantation
Association of Multicultural Affairs in Transplantation
Association of Organ Procurement Organizations
Chris Klug Foundation
Donate Life America
Donate Life Hollywood
International Society for Heart and Lung Transplantation
James Redford Institute for Transplant Awareness
National Minority Organ Tissue Transplant Education Program
National Donor Family Council
North American Transplant Coordinator's Organization
Organ Procurement and Transplantation Network
Organ Donation and Transplantation Alliance
Scientific Registry of Transplant Recipients
Transplant Recipients International Organization, Inc.
TransWeb
United Network for Organ Sharing

Organ transplants work, but there's still a shortage of donors

2011-03-27T06:30:00.000-04:00

By Amanda Korman, Berkshire Eagle Staff

Posted: 03/23/2011 12:34:41 AM EDT

Wednesday March 23, 2011

PITTSFIELD -- Among the patients in the dialysis unit at Berkshire Medical Center, Jeff Doscher knows he is lucky: He can still walk and still work. But, like everyone in his shoes, he is waiting to close the chapter of his life where he has to sit in the hospital three times a week to filter his blood for four hours.

The only way out of dialysis is an organ transplant, a long process of waiting and fingers-crossing that was the subject of Berkshire Community College's "Live to Tell: Priceless Gifts" forum on Tuesday afternoon.

In the U.S., 110,000 people are now on a transplant list, and 6,000 die every year while waiting, according to Sean Fitzpatrick, director of public affairs of the New England Organ Bank.

"It's simply a lack of donated organs," Fitzpatrick said.

Fitzpatrick joined two Berkshire natives on an expert panel at BCC to promote awareness about the need for people to join the donation registry.

"It's the people that have the little hearts on their driver licenses; you're my heroes," said panelist James Lambert, a chef in Lee who was the recipient of a liver transplant after six years on the waiting list.

Doscher, who is the dean of institutional advancement at BCC, sat in the audience among the numerous staff, students and community members who came for the event. He has polycystic kidney disease and has been on dialysis for more than two years.

Read More

Intellikine, PKD Foundation to investigate novel therapies for patients with PKD

2011-02-24T06:01:00.001-05:00

11. February 2011 00:23

Intellikine, a leader in the development of small molecule drugs targeting the PI3K/mTOR pathway, and the PKD Foundation today announced a collaboration to investigate novel, orally-available small molecule kinase inhibitors of the TORC1 and TORC2 complexes as a potential treatment for patients with polycystic kidney disease (PKD).

Click here to read the rest:

Good Fat, Bad Fat: Being Kidney Smart About Your Diet

2011-02-11T09:39:00.002-05:00

By: Wade Meredith

Fats are an essential part of the diet. They aid the absorption of certain vitamins, help maintain the integrity and function of cell membranes, and support the immune system. Too much dietary fat can contribute to heart disease, diabetes, obesity and certain cancers. Recent research on animal models of PKD reveal a correlation between both quantity and quality of fat in the diet on disease progression, including kidney size, amount of scar tissue and rate of decline in kidney function. Let's take a look at several types of fats and how they can affect your health and the health of your kidneys:

Read more: http://www.articlesnatch.com/Article/Good-Fat--Bad-Fat--Being-Kidney-Smart-About-Your-Diet/772237#ixzz1Df43sjhG
Under Creative Commons License: Attribution No Derivatives

More frequent dialysis improves lives, study finds

2011-02-07T09:13:00.002-05:00

CTV.ca News Staff

Updated: Sat. Jan. 22 2011 5:32 PM ET

For the 38,000 or so Canadians living with kidney failure, only dialysis three times a week keeps them alive. But a new study finds that dialysis every day, for a shorter period, seems to greatly improve quality of life.

The frequent dialysis idea has been suggested before, but has never been widely adopted. This new study in the New England Journal of Medicine may change some minds.

According to statistics released earlier this week, the number of Canadians living with kidney failure has more than tripled in Canada in the last 20 years. About a third of the cases are caused by diabetic kidney disease, while another 15 per cent are attributed to renal vascular disease.

Other reasons for kidney failure include autoimmune diseases such as lupus, and polycystic kidney disease.

Since 1965, the only way to keep kidney failure patients alive is through dialysis three times a week, for four hours at a time. But patients have long complained that while dialysis lets them survive; they still feel continually exhausted. That's what Ollie McKelvey remembers feeling.

"Technically, I lived to dialyze," she told CTV News. "I was just surviving."

But McKelvey recently took part in a study of a new program that had patients undergo dialysis more often but for shorter bursts: two hours a day, six days a week. McKelvey says the new approach changed her life.

"I found myself after the first week with a lot more energy, and just feeling human again," she says.

Dr. Rita Suri from the division of Nephrology at the University of Western Ontario took part in the study and says her research team found that more frequent and shorter dialysis treatment improved the quality of life and survival rates of patients.

Patients showed improvements to their heart function, which is often compromised during kidney failure, and improvements to their blood pressure. What's more, most receiving the more frequent dialysis reported feeling much better overall.

"I was quite surprised as to the magnitude of the change that patients felt significantly better," says Suri.

"Patients on frequent dialysis are able to walk better, have fewer symptoms, and able to do their day-to-day activities a lot better."

Doctors think more frequent dialysis acts better because it replicates what it's like to have a real kidney.

Previous research has also come out in favour of more frequent dialysis. And yet, most kidney patients are still treated according to the traditional schedule of three times a week. The problem, it seems, comes down to cost. Standard dialysis costs about $60,000 per patient per year. Doubling the frequency would double the cost.

Still, some doctors are trying to persuade provinces to expand dialysis services to offer more frequent treatments to more patients either in hospital or at home, noting that it will lead to lower health care costs down the line.

"We can improve the probability of survival with more frequent dialysis," Dr. Robert Lindsay of the Lawson Health Research Institute in London tells CTV. "This is a major thing."

More importantly, says Lindsay, is the quality of life benefits. He notes that most of the patients who received the more frequent dialysis begged his research team to let them stay on the program and not return to standard dialysis after the study was over.

"I didn't want to because I felt so much better," says McKilvey.

In fact, McKilvey decided to learn how to perform dialysis on herself at home where she now does it every day, vowing she'll never return to dialysis the old way.

With a report from CTV medical specialist Avis Favaro and producer Elizabeth St. Philip

Click below for video link:
CTV News: Avis Favaro on better dialysisResearchers in London, Ont. find people who are given dialysis six times a week as opposed to three times have lower blood pressure, fewer toxins in their blood, and better heart function.

CTV© 2010 All Rights Reserved.

Acute kidney injury due to osmotic nephrosis following intraoperative placement of an intraperitoneal antiadhesive barrier.

2011-01-25T13:45:00.000-05:00

Am J Kidney Dis. 2011 Feb;57(2):304-7.

Acute kidney injury due to osmotic nephrosis following intraoperative placement of an intraperitoneal antiadhesive barrier.
Economidou D, Stavrinou E, Giamalis P, Dimitriadis C, Economou S, Memmos D.

Department of Nephrology, Aristotle University of Thessaloniki, Hippokration Hospital, Thessaloniki, Greece.

Abstract
In recent years, a common strategy for the prevention of postsurgical intra-abdominal adhesions has been intrasurgical placement of adhesion barriers into the peritoneal cavity. Osmotic agents, such as various polysaccharides, frequently are used as antiadhesive materials. The effects of these materials on kidney function have not yet been studied. We report a case of an individual with pre-existing chronic kidney disease who developed acute kidney injury after surgical placement of an antiadhesive barrier of macromolecular polysaccharides. A kidney biopsy, performed because of persistent kidney failure, showed tubular cell lesions compatible with osmotic nephrosis lesions. This case suggests that use of polysaccharide-containing antiadhesive barriers can induce severe kidney damage. Such barriers should be used with caution in patients with abnormal kidney function to prevent irreversible damage.

Copyright Â© 2011 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
PMID: 21251542 [PubMed - in process]

Novel targets for the treatment of autosomal dominant polycystic kidney disease

2010-02-24T07:02:00.000-05:00

Expert Opin Investig Drugs. 2010 Mar;19(3):315-28.

Novel targets for the treatment of autosomal dominant polycystic kidney disease.
Belibi FA, Edelstein CL.

University of Colorado Denver, Division of Renal Diseases and Hypertension, Box C281, 12700 East 19th Ave, Aurora, CO 80045, USA.

IMPORTANCE OF THE FIELD: Autosomal dominant (AD) polycystic kidney disease (PKD) is the most common life-threatening hereditary disorder. There is currently no therapy that slows or prevents cyst formation and kidney enlargement in humans. An increasing number of animal studies have advanced our understanding of molecular and cellular targets of PKD. AREAS COVERED IN THE REVIEW: The purpose of this review is to summarize the molecular and cellular targets involved in cystogenesis and to update on the promising therapies that are being developed and tested based on knowledge of these molecular and cellular targets. WHAT THE READER WILL GAIN: Insight into the pathogenesis of PKD and how a better understanding of the pathogenesis of PKD has led to the development of potential therapies to inhibit cyst formation and/or growth and improve kidney function. TAKE HOME MESSAGE: The results of animal studies in PKD have led to the development of clinical trials testing potential new therapies to reduce cyst formation and/or growth. A vasopressin V2 receptor antagonist, mTOR inhibitors, blockade of the renin-angiotensin system and statins that reduce cyst formation and improve renal function in animal models of PKD are being tested in interventional studies in humans.

PMID: 20141351 [PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/20141351?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=2

Da Vinci Robot peels grape

2009-05-05T10:07:00.000-04:00

No health insurance? Get help here

2009-02-14T09:13:00.002-05:00

From Cnn
Click below for full story.
http://www.cnn.com/2009/HEALTH/02/12/ep.health.insurance.help/index.html
Negotiating with doctors and hospitals is just one thing you have to learn how to do when your insurance disappears, says Steve Luptak, executive director of an assistance group called Healthcare Advocacy. "I've had so many people who've just been laid off coming to me for help because they've lost their insurance. They're so stressed, they're so depressed, they feel like it's the end of the world," he says. "But there are things you can do. It's not a futile situation," he says. Watch for more tips for the uninsured »
If you want to try to get new, affordable insurance, or find programs that offer you financial help for doctor's visits, prescription drugs and more, follow these steps:
Step 1: Get good advice
When you get laid off and lose your health insurance, you may need someone in your corner. Several places specialize in helping people find new, affordable insurance and free care:
Healthcare Advocacy
Patient Advocate Foundation
Patient Services Incorporated
Step 2: Search for affordable insurance
With advice from experts at the groups above, begin your search for affordable insurance. Start with COBRA, which means you continue with your employer's insurance, except now you're paying the entire premium on your own. You can learn about COBRA at the Department of Labor's Web site.
If you can't afford to go on COBRA, you're in good company; a recent study by the Commonwealth Fund found that only nine percent of people who are offered COBRA actually use it. Sometimes it's less expensive to buy your own insurance policy rather than going on COBRA. You can compare prices at ehealthinsurance.com.
Step 3: Get your child on SCHIP
Even if you have too much money to qualify for Medicaid, your children may qualify for SCHIP, the State Children's Health Insurance Program. Here's a state-by-state directory of SCHIP programs.
There are other government programs, too. Your entire family may qualify for insurance from a state high-risk pool if you live in a state that has one.
If you think you might quality for Medicaid, see this state-by-state Medicaid directory.
Step 4: Get help with prescription drugs
If you can't afford health insurance -- or if your insurance doesn't include good prescription drug benefits -- look for $4 generic drugs at many major supermarkets and drug stores. Also, your state may offer a discount drug program (after you click, scroll down to see Table 2). You can also check these private groups that offer prescription assistance.
HealthWell Foundation
FamilyWize discount drug card
Needy Meds
Rx Assist
Rx Hope
Chronic Disease Fund
Partnership for Prescription Assistance
The Access Project
Step 5: Find financial assistance for your particular disease
Many diseases have specific foundations that offer financial assistance.
Heart Disease: Heart Support of America
Kidney Disease: American Kidney Fund
HIV/AIDS: The Access Project
Hepatitis: The Access Project
Cancer: see this Empowered Patient for a list of services
Alpha-1 Antitrypsin Deficiency, Chronic Granulomatous Disorder, Huntington's Disease, Idiopathic Pulmonary Fibrosis, and Pulmonary Arterial Hypertension: Caring Voice Coalition
Other rare diseases: National Organization for Rare Diseases
Vision Care: EyeCare America and Vision USA
Step 6: Find free clinics
Federally funded health centers offer free care in both urban and rural areas. Put in your address here and find one near you.

Kidney News PKD Blog

2009-01-24T09:14:00.001-05:00

Plexxikon and Roche Enter Second Partnership to Develop PLX5568 ...WELT ONLINE, Germany - Jan 8, 2009... partnership will be the development of this small molecule inhibitor of Raf kinase as an oral therapeutic treatment for polycystic kidney disease (PKD). ...Roche, Plexxikon In Drug Deal Potentially Worth $335 Million EasyBourse.comRoche and Plexxikon Sign Agreement To Jointly Develop Polycystic ... RTT NewsPlexxikon teams up with Roche, eyes $335M to fight kidney disease VentureBeatFierceBiotech - TMCnet all 22 news articles » OTC:RHHBY

Local kidney recipient wants incentives for organ donationsBaltimore Examiner, MD - Jan 21, 2009"People will do it if they are related, and then beyond that, it takes a heap of altruism," said Jones, of Sparks, who has adult polycystic kidney disease. ...

Extremely Great and Incredibly CheapTheStranger.com, WA - Jan 21, 2009The history combined with a CAT scan showed the hereditary polycystic kidney disease, which can cause brain aneurysms. (The patient's mother had died of an ...

Net service offers chance to save lifeLos Angeles Daily News, CA - Jan 18, 2009"Our brother needs a kidney transplant because he has polycystic kidney disease," Regina wrote on the site. "Unfortunately all of his siblings were ...

ARDvark Blog Journal of Adhesion Related Disorder: Are you registered and ready to Vote!

2008-10-03T18:45:00.000-04:00

ARDvark Blog Journal of Adhesion Related Disorder: Are you registered and ready to Vote!

ARDvark Blog Journal of Adhesion Related Disorder: Healthcare and social security McCain vs. Obama

2008-10-02T17:03:00.000-04:00

ARDvark Blog Journal of Adhesion Related Disorder: Healthcare and social security McCain vs. Obama

Kidney News PKD Blog

2008-09-22T11:51:00.001-04:00

Tengion Announces Expanded European Orphan Medicinal Product Designation For Neo-Bladder Augment
22 September 2008
Tengion Inc., a clinical stage regenerative medicine company focused on the development of neo-organs and neo-tissues, today announced that the European Medicines Agency (EMEA) and the European Commission (EC) have formally...[read article]

Scientific Abstracts On Cystinosis Research Are Published In October Issue Of Pediatric Nephrology

Gyrus ACMI, An Olympus Company, Launches Lightweight & Ergonomic, Digital Nephroscope

Elevated Levels Of Uric Acid In Healthy People Suggests A Greater Risk Of Developing Kidney Disease

New Gene Variant Identified For Non Diabetic End Stage Renal Disease In African Americans

Stateline.org Examines State Ballot Measures Related To Health Care

Initiatives Seek To Raise Health Awareness Among Hispanics, Educate Blacks About Chronic Diseases, Recognize Culturally Tailored Insurance Programs

Gordon Brown Praises NHS Staff On Reductions In C. Difficile And MRSA Infections, UK

High Blood Pressure Takes Big Toll On Small Filtering Units Of The Kidney

Pepperoni Pizza And Pelvic Pain

Kidney Headlines PKD Blog

2008-09-09T07:01:00.001-04:00

Plexxikon Initiates Phase 1 Trial for PLX5568 - First-in-Class Drug For The Treatment of Pain and Polycystic Kidney Disease

New Solution For Malnourished Dialysis Patients

Study Points To One Cause Of Higher Rates Of Transplanted Kidney Rejection In Blacks

Robotic Kidney Removal Performed In Michigan

Hope rekindles for chronic kidney disease patientsVanguard, Nigeria - 11 hours agoThe potential for seals composed of the patient’s native tissue to reduce the inflammatory response may translate to a decrease in post-surgical adhesions.

Coated Catheters Reduce Infection Risk

American Kidney Fund's Disaster Relief Program Available To Dialysis Patients

Improved Understanding Of Kidney Diseases

ARDvark Blog Journal of Adhesion Related Disorder: FDA:Potential Signals of Serious Risks/New Safety Information Identified by the Adverse Event Reporting System (AERS)

2008-09-06T14:34:00.000-04:00

ARDvark Blog Journal of Adhesion Related Disorder: FDA:Potential Signals of Serious Risks/New Safety Information Identified by the Adverse Event Reporting System (AERS)

Kidnay News PKD Blog

2008-05-28T10:15:00.000-04:00

Op-Eds Address Presidential Candidates' Health Care Proposals

For Dialysis Patients, Catheterization Sites Do Not Carry Very Different Infection Risks
Preclinical Data Demonstrate Ability To Regenerate An Entire Bladder With Tengion Neo-Bladder Replacement(TM)

Access To The Bloodstream For Kidney Dialysis Not Improved By Reducing Blockage

Patients With Acute Kidney Injury Do Not Have Improved Outcomes With More Intensive Dialysis

Risk Of Diabetes May Be Increased By Anti-Rejection Drug Administered After Kidney Transplant

Striving Toward Better Diagnosis And Treatment Of Liver Diseases

Black Patients Face Higher Rates Of Death In Early Stages Of Chronic Kidney Disease

Prospective Study Of The Long-Term Effects Of Shock Wave Lithotripsy On Renal Function And Blood Pressure

Risk Of Death In Patients Waiting For Kidney Transplants Increased By Hidden Heart Condition

Vitamin D Linked To Reduced Mortality Rate In Chronic Kidney Disease

Plexxikon Presents Positive Results From Preclinical Kidney Disease Study

2008-05-28T10:13:00.000-04:00

Posted on: Thursday, 22 May 2008, 11:52 CDT
Plexxikon has announced positive data from preclinical studies of polycystic kidney disease demonstrating significantly reduced kidney disease following treatment with Plexxikon's novel drug candidate.
In the preclinical study of Plexxikon's polycystic kidney disease (PKD) drug candidate, doses of the drug candidate were administered orally daily for 14 days. A marked reduction in kidney cyst burden was observed in the treatment group compared to vehicle treated mice.

Levels of blood urea nitrogen, an indicator of kidney function, were also significantly improved in the drug-treated groups compared with the vehicle-treated group, suggesting that improved renal function accompanied reduced cyst growth in treated animals.
Plexxikon's novel small molecule kinase inhibitor is said to be a highly selective and potent inhibitor of Raf kinase, a critical mediator of PKD pathology.
Source: Datamonitor

Kidney Blog PKD Blog

2008-05-22T16:38:00.000-04:00

Cardiac Rhabdomyoma and Renal Cyst in a Fetus Early Onset of ...Journal of Ultrasound in Medicine (subscription) - 3 hours agoA postmortem examination showed polycystic kidney disease (PKD) and a cardiac rhabdomyoma, which is a prenatal marker of TSC. On the basis of the maternal ...

Yale's Rosenbaum Honored by University of SienaMedia Newswire (press release), NY - May 16, 2008Notable among disorders related to defective cilia are

Plexxikon Announces Preclinical Data Demonstrating Dramatic ...Business Wire (press release), CA - May 21, 2008These data were recently presented at the ISN Forefronts Symposium on Polycystic Kidney Disease in Montreal, Canada by Stefan Somlo, MD, CNH Long Professor ...

Kidney Headlines PKD Blog

2008-03-25T06:37:00.001-04:00

St. Jude Study Offers New Hope For Children With Kidney Tumors Deemed Inoperable

Transplant Societies Protest FDA Policy In American Journal Of Transplantation

LifeCycle Pharma Announces Positive Top-Line Results Of Phase II Clinical Trial Of LCP-Tacro In Stable Kidney Transplant Patients

PLC Systems Receives FDA Approval To Commence Pivotal Study Of RenalGuard(TM) In The U.S.

Novel Discovery By Einstein Scientists Could Lead To Much-Needed Treatment For Kidney Failure

Avera Medical Minute: National Kidney Month

2008-03-25T06:36:00.000-04:00

The rate of kidney disease has jumped significantly in this county since the Mid-1990's. Up 30%, an estimated 26 million people are living with chronic kidney disease. Since it's National Kidney Month, we talked to a Northwest Iowa woman who is living proof that living donors can make a world of difference.
Five years after Carol Boote from Hull, Iowa got the gift of life, the staff at Avera North Central Kidney Institute say she is the poster child for kidney transplants.
Nephrologist Dr. Tina Melanson says, "She has a wonderful life. So much better than the quality of life she would have on dialysis. And transplant for anyone, including Carol, offers a reasonable life expectancy, a normal life expectancy that would not be achievable on dialysis."
Carol was born with polycystic kidney disease, but doctors didn't discover it until she was treated for a kidney stone and that's when they noticed her kidney's were growing abnormally.
Carol says, "I was just this normal person who had kidney disease. It's hereditary but no one in my family had it. I didn't have diabetes, I was never on dialysis. I was lucky that way. They were able to track it for 15 years and before I needed a transplant."
When the time came, she says any one of her family members would have given her a kidney, but it was her sister she had an unspoken agreement with. She gladly gave up hers.
Carol says, "My sister Carla and I are only 15 months apart and all through our lives we've been like this (she holds up her index finger next to her middle finger). We were together all the time. If she was going out on the boat for the weekend I would joke with her to be careful. I might need that kidney today. "
Now part of Carla is always with Carol and Carol says she feels a million times better.
Read the Rest

Kidney Headlines PKD Blog

2008-03-10T07:15:00.000-04:00

NovaBay Pharmaceuticals Commences Phase I Human Clinical Trial For The Prevention Of Catheter Associated Urinary Tract Infections

Analysis Of A Computer Based Simulator As An Educational Tool For Cystoscopy: Subjective And Objective Results

Beyond The Abstract: Reliability Of The 24 H Sensation Related Bladder Diary In Women With Urinary Incontinence

Laboratory And Clinical Development Of Single Keyhole Umbilical Nephrectomy

Followup Of Patients With Interstitial Cystitis Responsive To Treatment With Intravesical Bacillus Calmette Guerin Or Placebo

Fresenius Medical Care Offers Tips For National Kidney Month

Bacteria May Reduce Risk For Kidney Stones

Risk Of Death From Acute Kidney Failure Reduced By 'Renal Assist Device'

Chronic Kidney Disease - Europe's Silent Epidemic

New Awareness And Prevention Series For Community Health Events Released By NIDDK

American Association Of Kidney Recognizes March As Kidney Disease Awareness Month

Kidney Stone Research To Be Aided By Mouse Model

SCORED Screening Test Accurately And Efficiently Identifies Individuals With Silent Chronic Kidney Disease

Transplantation Boosts Survival Rates For Young Kidney Failure Patients, Canada

LifeCycle Pharma Announces Positive Top-Line Results Of Phase II Clinical Trial Of LCP-Tacro In Stable Kidney Transplant Patients

Race, Insurance Status Affect Access To Transplantation And Kidney Disease Treatment

World Kidney Day is Coming

2008-03-10T07:14:00.000-04:00

How Are Your Kidneys Doing?
You know when you have a headache, sore throat, a cold or the flu. But would you know if your kidneys weren't working? High blood pressure and diabetes can damage your kidneys without any warning. If you're one of the millions of Americans who has chronic kidney disease and doesn't know it, March 13 or World Kidney Day, may be the day that saved your life. Check out your kidneys with a free screening and take the kidney quiz to learn more.
NKF
_______________________________________
Don’t Take Kidney Health for Granted
Learn about Amazing Life-Sustaining Kidneys this March
In a popular 1970 song, singer-songwriter Joni Mitchell asked, “Don’t it always seem to go that you don’t know what you’ve got till it’s gone”—a question that could have been aimed at people with chronic kidney disease (CKD). The kidneys play a crucial role in maintaining overall health but are rarely appreciated until they become damaged and can no longer do their jobs.
Unless Americans start doing more to protect kidney health, untold millions could soon be singing the same sad song. Recent studies indicate that 26 million adults suffer from CKD and that this number is likely to increase in the future. To raise awareness during National Kidney Month (March, 2008) and to mark World Kidney Day (March 13), the National Kidney Foundation offers a list of 10 key functions healthy kidneys perform.
For more information, click here .
NKF

Kidney News PKD blog

2008-02-29T07:40:00.002-05:00

Race, Insurance Status Affect Access To Transplantation And Kidney Disease Treatment
______________________________________

Funding helps patients receive treatment at home
Published: 29 February, 2008
SPENDING long hours hooked up to a haemodialysis machine is bad enough, but travelling miles for the privilege makes it even worse.
Yet that is the fate of most patients from the North who regularly have to make long journeys to Raigmore Hospital in Inverness, or its satellite units, to undergo dialysis.
But Spinningdale woman Glenys Munro has just been given the opportunity to undergo the lifesaving treatment – which removes harmful wastes from the blood, built up as a result of kidney failure – in the comfort of her own home.She is one of a handful of selected Highland patients to benefit from around £30,000 recently made available by NHS Highland.
The funding has enabled rooms in their homes to be converted and fully equipped as a dialysis suite. It has also led to the appointment of a dedicated home haemodialysis nurse, Chris Ridden, who is overseeing the new project.
Extensive work, including new flooring and fitting power points and plumbing, has just been completed at Keas Cottage where Glenys lives with her young daughter, Lynn.
Her consultant renal physician at Raigmore, Dr Stewart Lambie, is excited about the move to haemodialysis at home but said that, far from being a new development, it represented a turning back of the clock.
He explained: "When dialysis first started back in the 1970s everyone was on home haemodialysis, but then it swung away to hospital-based treatment.
"Now it's swinging back again, and just recently there has been a recognition that dialysing people more frequently at home is better for them."
Dr Lambie explained that Glenys and the other patients were chosen because they fitted certain criteria and were thought to have the most to gain.
"We've selected those who live furthest away from a dialysis centre who are going to be fit enough and able to learn how to set the machine up," he said.
"It's quite demanding for the patient to learn how to do it, but they have a lot to gain. Home haemodialysis is a lot more flexible and patients can undertake it whenever they like.
"They will also have more dialysis. Instead of the four hours, three times a week, hospital patients currently receive they will be able to do three hours, six times a week, which will make a huge difference to them.
"More frequent dialysis will mean they need to take fewer tablets and will also give them more energy and a better appetite."
Glenys, who works part-time at Mark Banham's tree nursery, had been suffering from frequent headaches and high blood pressure for some years before being diagnosed with polycystic kidney disease in 2000.
She said: "I'm delighted to have been given this opportunity. It's a lot more convenient as I will be home for my daughter and will also be able to continue working. I am being given the chance to live as normal a life as possible."
She paid tribute to her daughter Lynn and sister Heather, a local nurse, without whose support she said she would be unable to carry out home dialysis.
The home haemodialysis project will be assessed once it has been running for a while, and it is hoped further funding will be forthcoming to extend it to include more patients from the North.
"We have plans to significantly increase our home haemodialysis programme," said Dr Lambie.
Source

Erma Bombeck

2008-02-27T06:51:00.000-05:00

Born in Dayton, Ohio, Bombeck graduated from the University of Dayton in 1949 with a degree in English. She started her career in 1949 as a reporter for the Dayton Journal Herald, but after marrying school administrator Bill Bombeck, a college friend, she left the job and raised three children.

As the children grew she started writing At Wit's End, telling self-deprecating tales about the life of a housewife. It debuted in the Kettering-Oakwood Times in 1964. She was paid $3 per column.

Growing popularity led At Wit's End to be nationally syndicated in 1965, and eventually it ran three times a week in more than 700 newspapers. The column was collected in many best-selling books, and her fame was such that a television sitcom was based on her. The series, Maggie, ran for eight shows in 1982 before being cancelled.

In 1971, the Bombecks moved to Paradise Valley, Arizona.

Bombeck had autosomal dominant polycystic kidney disease. In 1996 worsening health forced her to have a kidney transplant, and she died of complications that year. She is interred in the Woodland Cemetery, Dayton, Ohio.

02/21/08

New Device to Track Organ Health

2008-02-27T06:50:00.000-05:00

New Device to Track Organ Health
Research by Basque scientists has led to a patented device, which measures the electric impedance and temperature of organs before transplantation, and can supposedly provide guidance as to the health of the organs.
By means of a microelectrode that measures the impedance and temperature of the tissues, the system enables the state of any organ to be monitored from the moment of its extraction, during its transport, to the moment of the surgical operation to transplant it into a patient.
The Ikerlan-IK4 device, designed in collaboration with the National Centre for Microtechnology (CNM-CSIC) and the Carburos Metálicos company and patented in conjunction with I2M Design S.A., uses a polymer substrate that represents a great advance in biomedical instrumentation, as it does not produce injury in the tissues during transport or surgical manoeuvres. It even opens a new way to control organ rejection, given that the microelectrode can remain implanted for a considerable time without causing injury.
The application has a number of prototypes already and has had clinical trials with organs of animals at Barcelona’s Hospital Clínic. Moreover, it is of particular interest for a process as delicate as an organ transplant, as it provides an objective indicator of the evolution of the organ in which, despite the conservation techniques used – whether with special liquids or in cold -, the duration of the viscera is highly limited (12 hours in the case of the kidney, eight for the liver and only four hours in the case of the heart). The device is used incorporated into a small electronic system which gathers and sends data by telemetry to an external system, enabling the verification of the state of the organ at all times.
Press release: Ikerlan-IK4 (CIC microGUNE Microfluidics Unit) patents device that measures optimum state of an organ prior to transplanting

Kidney Headlines PKD Blog

2008-02-26T10:25:00.000-05:00

Diazyme Introduces New Test For The Early Detection Of Kidney Disease

Repros' IND For The Commencement Of Phase III Studies Of Proellex(R) In The Treatment Of Anemia Associated With Uterine Fibroids Is Now Effective

Hyaluronan Treatment Of Interstitial Cystitis/Painful Bladder Syndrome

Calcineurin Inhibitor-Sparing Regimens In Solid Organ Transplantation: Focus On Improving Renal Function And Nephrotoxicity

Kidney Donor Age Linked To Aortic Stiffening

The National Kidney Registry And NewYork-Presbyterian Hospital/Weill Cornell Medical Center Announce A Triple Swap Starting A Donor Chain

American Nephrology Nurses' Association Announces National, Regional Election Results

New Independent Research Study Indicates That Cylex's ImmuKnow Test May Identify Kidney Transplant Patients At Risk For Early Acute Rejection

No Real Differences Noted In Kidney Failure Treatments

Before A CT Scan, Many Should Take Drug To Protect Kidneys

Stowers, KU Med scientists get grants to study kidney disease

2008-02-26T08:54:00.000-05:00

The PKD Foundation has given a two-year, $150,000 grant to a scientist at the Stowers Institute for Medical Research and a $50,000 fellowship to a University of Kansas Medical Center reseacher, both to study polycystic kidney disease.
The grants are part of $4 million the Kansas City-based foundation will spend on research in 2008.
Xiaogang Li, a senior research associate in the Stowers Institute's Rong Li Lab, will study the role of a number of enzymes, called histone deacetylases (HDACs), which play a role in cell-cycle regulation and in the formation and breakdown of cilia in the kidneys, the institute said in a release. Mutations that affect the function of cilia cause PKD. New information about the function of HDACs in cells may enable the identification of new treatment targets in PKD.
The fellowship will go to Cibele Pinto at the University of Kansas Medical Center's Kidney Institute, Amy Freaney, coordinator of the foundation's grants and fellowships program, said Thursday.
Polycystic kidney disease is one of the most commont life-threatening genetic diseases, the institute said. Dialysis and transplantation are the only treatment options for kidney failure, and the disease has no known cure.
"Xiaogang Li is a very dedicated scientist who has made important contributions to the research on Autosomal Dominant Polycystic Kidney Disease," Rong Li, a Stowers Institute investigator, said in the release. "This grant will enable him to continue his original work to understand the disease mechanism and to identifynewpossibilitiesfor disease treatment."
http://www.bizjournals.com/kansascity/stories/2008/02/18/daily30.html

Clinic targets disease in children

2008-02-26T08:53:00.000-05:00

By KAWANZA NEWSON
knewson@journalsentinel.comPosted: Feb. 17, 2008New parents often spend the first year of their child's life anticipating milestones such as smiling, babbling and rolling over onto their tummies.
But for Jennifer and Jeff Roubik, those moments never came. Instead, their son lay listless. His skin was tinted gray as his kidney function rapidly deteriorated from a genetic disorder called autosomal recessive polycystic kidney disease.At 3 months, Gabriel had one kidney removed. A month later, he lost his second kidney and began dialysis. Each day, his parents wondered if their son would make it to his first birthday."Those thoughts kept coming in," said Jeff, 37, of Elkhorn. "He also had heart problems because his blood pressure was out of control. Things were not pretty."Though researchers still don't understand what causes most pediatric kidney disorders, the opening of a nephrology clinic and lab at the Children's Research Institute affiliated with Children's Hospital in Wauwatosa will soon provide some answers.Using a $4.6 million grant from the National Institutes of Health, a group of Medical College of Wisconsin researchers will design studies to better understand the basic molecular and cellular mechanisms associated with pediatric kidney disease so they can develop therapies to prevent and treat the condition.This work will then be quickly translated into clinical trials using childhood kidney disease patients."This is a very exciting time," said Ellis D. Avner, director of the Children's Research Institute and associate dean of research at the Medical College. Read More

In His Own Words: A Donor's Experience

2008-02-25T10:36:00.000-05:00

At a recent Walk for PKD, my wife and I stopped at the transplant information table and talked to the lady at the table and some others who stopped by. They were all organ recipients, or potential recipients, and shared their experiences and conditions. It was amazing how different their experiences were. Listening to others made me appreciate our transplant experience, which I would like to share from another perspective. I was my wife's living donor and want to encourage others to consider this option and let them know what to expect.
It's been over a year since I donated a kidney to Cris. My wife suffered from Polycystic Kidney Disease and was getting close to renal failure in the fall of 2005. She suffered chronic discomfort and was subject to numerous kidney and urinary tract infections for several years. Her kidneys were very large and covered with cysts. Cris' mother suffered from the same disease and went through years of dialysis and a failed transplant, so we were familiar with our options. Cris' condition required the removal of her kidneys before a transplant could be performed. This created some timing issues that we wanted to avoid. The kidneys would have to be removed and a recovery period would be required, then she would have to be put on the waiting list for a kidney. This could result in years of dialysis. I told Cris I wanted to be tested as a possible donor. This way, everything could be planned and scheduled. OrientationWe live in Winston-Salem, North Carolina and Cris was lucky enough to be a patient of Wake Forest University Physicians and North Carolina Baptist Hospital. The system this transplant team employs seems more patient-friendly than those described by other transplant patients. We attended an orientation presented by a transplant coordinator that included videos, handouts, and details and tips from some of her past experiences with other transplants.
We also met with a social worker. He was trying to determine if Cris was a good candidate for a transplant from an emotional point of view. How did she feel about another person's organ inside of her body and would she follow the doctors' instructions and regularly take her medication? I was given a two-page list of all of the possible negative outcomes from donating in order to test my resolve. We were told that donors sometimes change their minds at the last minute, and part of this interview was to make sure I wouldn't. The majority of these risks are consistent with those involved with any surgery that includes anesthesia. The only one I really had to consider was the risk that I might develop a kidney problem later in life. There is a history of high blood pressure and diabetes in my family, so it could be relevant. As always, people must weigh the risks when donating an organ.
Finally, we met with the financial representative from the hospital. She explained that Medicare covers the cost of the transplant and that Cris would remain covered for three years following the transplant. During this time, she could apply for the Medicare D prescription plan. She went over what was covered and all co-pays involved with the transplant. Her main objective was to make sure we could pay for Cris' prescriptions, since many transplant rejections are a result of a failure to take the medication. It's a shame that money is an issue when trying to extend a life or improve the quality of that life. There are a lot of economic considerations for the recipient, but this is about the donor experience. I never received a bill for anything related to my care from the initial test to my final check-up four months after the surgery.
Tests and Preparation From the information collected at these interviews, the transplant team decided that we were emotionally and financially equipped for the transplant. I was scheduled for a series of tests to determine if I was a match and healthy enough to donate. I had an EKG, a chest x-ray, and they drew nine vials of blood for tests. I was in the hospital less than two hours for all of this. We were a blood type match, matched 2 out of 6 antigens, and passed the cross-match test. It was a go!
At first, my meeting with my surgeon was not what I expected. He again made me aware of all of the risks. It was as though he was trying to talk me out of the operation. It was just one more test of my resolve, and once he was convinced, the examination proceded in a more positive light. He explained the procedure and the rest of the tests I would need. The donor is assigned a different surgeon than the recipient to reduce the likelihood of a conflict of interest. My welfare was the main concern of my doctor, just as my wife's health was her doctor's responsibility. There were two things he informed me of that concerned me I would have to get down to 220 pounds and deal with a catheter after the operation. Since I weighed over 260 pounds, I knew I had my work cut out for me. If I didn't lose the weight, he still might be able to remove the kidney, but not laproscopically. The risks and recovery time from laproscopic surgery are significantly less than with regular surgery.
From the information we read and discussions with our doctors, we learned that there are some advantages for the recipient of a kidney from a living donor over one from a cadaver. There is a lower rejection rate with a "live" kidney. The "live" kidney starts working easier because it is exchanged so quickly that it may not even stop functioning. Typically, the donor and the recipient are operated on in adjoining rooms separated only by a door. The donor goes in ahead of time, followed shortly by the recipient, and by the time the kidney is removed, the recipient is ready. It can be as short as ten minutes that the kidney is actually out of a body.
The final tests involved the injection of a fluid through an IV and the inspection of my kidneys at work. My kidneys were x-rayed before the fluid was introduced. After the fluid was injected, I was put into something similar to a CAT scan to examine my lower body. My kidneys were X-rayed again. I was asked to empty my bladder, and X-rayed one last time. Everything was fine.
Cris had her kidneys removed in March of 2006 and had about a two-month recovery period. By May, I had lost 40 pounds and was at 225. The doctor said this was close enough, so blood was drawn to verify one last cross-match test and the transplant team met to schedule the date for the operation.Surgery and RecoveryCris and I were admitted to the day hospital Monday afternoon for our Tuesday morning surgery. They took blood once again you have to get used to getting stuck. Since I wasn't going to get to eat the next day, the nurses brought me lots of snacks before my midnight deadline for eating and drinking. If you're donating an organ to your wife as I was, every female you come into contact with during this experience will think you're the nicest guy in the world and give you all the attention you want. We were on the same floor, so we spent some time together that night and Cris came to see me off when they came to get me about 6 a.m. I was taken to the preparation room where the anesthesia was administered and the next thing I remember was waking up in the recovery room with my daughters by my bed. Both of our surgeries were done and they told me Cris was doing fine, too.
When I woke up I was drowsy and drifting in and out. There was a device blowing oxygen below my nose. I can't tell you how long I spent in the recovery room. When I got into my regular room I felt no ill effects from the anesthesia, but was extremely thirsty.
Tuesday night I started to experience intense pain in my left shoulder. It scared me a little because I've always heard that pain in the left arm can be associated with a heart attack. The nurses and interns that visited had no explanation, but assured me there was nothing to worry about. It was particularly painful when I used the "incentive" breathing apparatus they give you to prevent blood clots in your lungs. I also received Hepron injections after the surgery to reduce the risk of blood clots. Wednesday afternoon I finally saw my doctor, who explained the pain. When they do the laproscopic procedure, the area of the surgery is inflated with gas to allow more work space. During recovery, this gas accumulates in the upper body, resulting in some pressure and consequently, some pain. I was scheduled to go home on Thursday, but had to stay and extra day because of a fever. The shoulder pain was gone by the next evening.
The most difficult part of the recovery was dealing with the healing of the six-inch or so incision made across the lower abdomen where the kidney was removed. Your doctor will want you to spend some time sitting up in a chair and walking as soon as possible. This was much easier after they removed the catheter Wednesday morning. There was no pain in having the catheter in or having it removed, it was just awkward to maneuver around with it in place. You can't really sit up, so you learn to get on your side and swing your legs to get in and out of bed. The first 24 hours I had a button that allowed me to dispense pain medication through my IV. I would give myself a dose before getting out of bed, but didn't need it when just lying in bed. They also wanted me to wear leg massagers whenever in bed, so I had to deal with getting them off and on every time I got up. It's the "sit-up" motion that is painful for a few weeks.
Long-Term RecoveryWe were both discharged Saturday morning. Fortunately, my sister came to stay with us for a couple of weeks during our recovery. I thought Cris and I would be able to handle all of the simple household tasks, but I was wrong. When you can't bend over or drive, and need to spend most of your time in a reclined position, you need some help. We'll never be able to thank her enough. The only medications I was given were a stool softener and some pain medication. For the first two weeks after the surgery, I found that I could sit up at the computer or watch TV for an hour or two, but then had to lie down for awhile. Cris and I would go for walks around our development, but it was pretty exhausting. After another two weeks, though, I was ready to return to work. Final ThoughtsI have described the details of my experience so that potential donors can know some of the things to expect. While I talk about some pain and complications, none of what I went through was severe enough to prevent me from doing it again (if I could) or recommending it to others. I will have my wife for many years to come, and my kids still have their mom. Cris will not have to endure the ordeal of dialysis and can experience a better quality of life. When people hear what I've done, they seem to be genuinely impressed with the generosity of my actions. That's nice, but if it inspires anyone else to do the same, it's great! I certainly didn't donate for any personal recognition - it's just the right thing to do for someone you love. Our social worker put another way that also makes the act worth doing. He said that donation of this type is like donating two kidneys one for Cris, plus the one that she would have gotten that went to someone else. I hope people out there will consider being a living donor.
Share your story with the PKD Foundation.

Kideny News PKD Blog

2008-02-12T10:20:00.000-05:00

AMAG Pharmaceuticals Provides Clinical Information On Ferumoxytol As An Intravenous Iron Replacement Therapeutic In Chronic Kidney Disease Patients

Intensive Insulin Therapy Protects Kidneys In Critically Ill Patients

When Kidney's Ability To Clean Its Own Filters Breaks Down, Disease Likely

4 Million Dollars Award To Improve Detection Of Acute Kidney Injury After Cardiac Surgery

Cleviprex Demonstrated Rapid, Precise Blood Pressure Control In High-Risk Patients, According To New Analyses

Studies On Urgent(R) PC To Be Presented At The 2008 Society Of Urologic Nurses And Associates Annual Symposium

Black Men Most Likely Kidney Disease Patients To Have Uncontrolled High Blood Pressure, Study Finds

Teva Announces Tentative Approval Of Generic Flomax(R) Capsules

Healthcare Providers Direct, Inc. Announces First Accurate And Effective Rapid Point-of-Care Screening Test For Microalbuminuria

Mechanisms Of Hemostatic Failure During Laparoscopic Nephrectomy: Review Of Food And Drug Administration Database

Kidney Patient Functioning With Donation from 2-Year-Old

2008-02-12T09:31:00.000-05:00

February 10th, 2008 @ 7:46am
by Associated Press
TUCSON, Ariz. (AP) _ It gave this kindly man pause _ that the two kidneys that could heal his body and give him a free and active life would come from such a young child.
But in yet another landmark organ transplant at University Medical Center, William Diehl _ a Willcox grandfather _ was given kidneys donated by a 2-year-old on the morning of Dec. 10.
``It kind of bothered me _ that the organs had to come from a baby,'' he said. ``I had to think about that.''
But the fact is that when transplant surgeons finally figured out that they actually could use these very small organs to save adult lives, it has put a small dent in the horrific shortage of donor kidneys in this country.
Right now, more than 74,000 people are waiting for kidneys. But fewer than a quarter will get one in the coming year.
``These baby-to-adult transplants are not frequently done _ usually at the major transplant centers,'' said Dr. Rainer Gruessner, University Medical Center's new chief of surgery. Gruessner has brought cutting-edge experience as an abdominal transplant surgeon to an effort to rebuild the hospital's transplant program.
``But the issue is so many patients waiting on the kidney list,'' he continued. ``Using these small donors for adults is one way to expand the kidney transplants we can do.''
For a man of 56, a single kidney from a child so small would not do the job. So surgeons instead transplant the child's entire kidney block _ the two kidneys connected by the major blood vessels _ into the adult.
This is known as an ``en-bloc'' kidney transplant _ a technically challenging and somewhat riskier surgery than the far more common transplant with a single adult donor kidney.
Only about 100 en-blocs are done per year in this country, using donors younger than 5. As the surgical techniques have improved _ to deal with hooking very small organs and vessels up to an adult-size body _ several studies have concluded that the operations are getting excellent results and should be done more often.
``In the current era of severe organ-donor shortage, use of en-bloc technique allows for valuable utilization of deceased donor kidneys that might otherwise be discarded,'' states an analysis of this transplant in a 2005 issue of the American Journal of Transplantation.
But chief among the en-bloc risks is a higher threat of a blood clot, which can be triggered by the child donor's very small blood vessels.
``That was the problem that caught my attention,'' said Diehl, who is doing so well post-transplant that he actually made a trip to Willcox a couple months ago.
Since the transplant, he no longer needs dialysis _ that three-times-a-week grind of hooking yourself up to a machine for several hours to do the work of failed kidneys. It's a tedious procedure that leaves patients drained of energy.
Diehl had been on dialysis for a year and a half _ ever since his kidneys failed due to polycystic kidney disease. He probably has had the disease all his life but was not diagnosed until he was nearly 40. He finally lost one kidney to the disease in May 2006, with the other all but dysfunctional.
Diehl, who has four grown daughters and seven grandchildren, is regaining strength and enjoying new freedom to be with his extended family.
``He's a basically healthy man in good shape, and we wanted to go ahead with this when the kidneys became available,'' Gruessner said.
``The whole aim of a kidney transplant is to get patients off dialysis, and we didn't want to wait,'' Gruessner said. ``With the donor shortage, that wait could have lasted many more months.''

Compound prevents cancer in lab

2008-02-11T09:34:00.000-05:00

James CoburnThe Edmond Sun
EDMOND — A culmination of 17 years of research has led scientists at the University of Oklahoma Health Sciences Center to discover a synthetic compound that prevents cancer in the laboratory.This discovery is not serendipity but a carefully controlled strategy, said Doris Benbrook, principle investigator and researcher at the OU Cancer Institute.Cancer kills more than 7,600 Oklahomans each year, according to the American Cancer Society.Oklahoma State University chemist Darrell Berlin synthesized compounds similar to vitamin A, but different by one atom. “I would take these compounds and test them on cancer cells and normal cells to try and find ones that would kill the cancer cells without harming normal cells,” Benbrook said.She modified the chemical structure of the compound to optimize the killing of the cancer cells and to avoid harming the normal cells. “It’s been changed so much that it’s no longer a vitamin A derivative,” she said.Planning clinical trials is part of Benbrook’s long-term goals with the compound. But FDA approval is needed and there is not yet a drug ready for testing. She will apply to the National Cancer Institute to support pre-clinical testing. Tests conducted by OU researchers have found the compound effective against all the 12 types of cancer they have used it on. Among the diseases and conditions being studied for treatment are polycystic kidney disease, kidney cancer and ovarian cancer.“The National Cancer Institute was impressed by lab findings — that (the compound SHetA2) can prevent transformation of normal cells into cancer cells,” she said.Testing costs millions of dollars and is required to start clinical trials, she said. More than $2 million already has been invested in the research.Cancer survivor Tammy Padgett of Edmond said federal funding for cancer research is critical for improving cancer treatments and in curing cancer.Breast cancer funding saved her life, said Padgett, whose type of breast cancer was successfully treated by the drug Herceptin. She celebrates being free of cancer for six years.Benbrook also envisions that the compound could lead to an application in treatment after primary surgery and chemotherapy to prevent the reoccurrence of the cancer.“Research will keep on going,” she said. “This is not the magic pill, but potentially another compound down the road might be the magic pill. But we know we’re going in the right direction.”GO TO http://w3.ouhsc.edu/benbrooklab for the Web page of Doris Benbrook’s lab.

Kidney News PKD Blog

2008-01-31T07:15:00.000-05:00

Portugal To Introduce A Bundled Rate For Hemodialysis Treatment

American Nephrology Nurses' Association (ANNA) Symposium To Highlight Innovative Approaches In Patient Care

Low Dose Computed Tomography For The Evaluation Of Flank Pain In The Pregnant Population

Low Dose Computed Tomography For The Evaluation Of Flank Pain In The Pregnant Population

Kidney Failure: Preference-Based Quality Of Life

A Miracle Cure For Women May Be Cranberries

Intensive Insulin Therapy Protects Kidneys In Critically Ill Patients

When Kidney's Ability To Clean Its Own Filters Breaks Down, Disease Likely

Reproductive issues for adults with autosomal dominant polycystic kidney disease.

2008-01-31T07:14:00.000-05:00

Vora N, Perrone R, Bianchi DW.
Department of Pediatrics, Tufts-New England Medical Center and Floating Hospital for Children, Boston, MA 02111, USA.
Autosomal dominant polycystic kidney disease (ADPKD) is a common disorder. However, the consequences of ADPKD on male and female reproductive health are not widely known. Several abnormalities are found in men with ADPKD, including necrospermia, immotile sperm, seminal vesicle cysts, and ejaculatory duct cysts. Female fertility is not affected. Affected women with ADPKD and normal renal function have a high rate of successful uncomplicated pregnancies. Pregnant women with ADPKD with compromised kidney function should be monitored carefully for the development of hypertension and preeclampsia. Their fetuses should be examined sonographically for signs of uteroplacental insufficiency, such as intrauterine growth restriction and oligohydramnios. The diagnosis of ADPKD should always be considered when prenatal sonographic findings of hyperechogenic enlarged kidneys are found. In this setting, a family history and renal sonogram of both parents is indicated. Sequencing of the PKD1 and PKD2 genes is available and can be used for both prenatal and preimplantation genetic diagnosis. We review in detail these topics to familiarize physicians taking care of patients with ADPKD with the reproductive issues that confront affected individuals.
PMID: 18215709 [PubMed - in process]

Scientist triumphs after setback in kidney transplant method

2008-01-30T08:56:00.000-05:00

By Patricia Wen
Globe Staff / January 24, 2008
Dr. David H. Sachs was full of optimism when the third patient in his $1 million study was wheeled into the recovery room at Massachusetts General Hospital after an experimental kidney transplant.
graphic Kidney donations
graphic Research team's approach
The first two patients had thrived, adding credibility to an unorthodox idea that Sachs had pioneered over his career, that transplanting a donor's bone marrow along with the kidney could solve the problem of organ rejection, sparing patients a lifetime of powerful antirejection drugs.
But 10 days after the third patient's surgery, Sachs's phone rang at his spacious lab overlooking Boston Harbor. A colleague reported that William Andrews, a 43-year-old father of two, was rejecting the kidney.
Sachs and his research team remember the darkness of the ensuing months in 2003, when they abruptly suspended their transplants for nearly two years. Andrews was demoralized and on dialysis, his sister's donated kidney seemingly wasted. Over and over, Sachs paced the corridors of his lab asking himself, "What did we miss?"
Today, capping a comeback from the crisis, Sachs and his team are reporting that they unraveled the explanation for Andrews's rejection. After they tweaked their protocol, adding a drug to avert what happened to Andrews, two new patients have thrived without the long-term need for antirejection drugs, according to a paper published in the New England Journal of Medicine.
Overall, four of Sachs's five patients have experienced no organ rejection, a particularly striking accomplishment because they all received kidneys that were different from their own tissue type. Transplants of such mismatched organs are the most common and the most likely to be rejected, even when patients take immunosuppressive drugs.
"I had confidence we would figure it out," said the 66-year-old Harvard Medical School professor, who has dedicated more than three decades to conquering organ rejection. He said the results restored his faith that his once-radical idea will eventually become mainstream, making organ transplants safer and more available.
Transplant surgeons said Sachs's study represents a pivotal moment in organ transplantation, demonstrating that it is feasible to eliminate immunosuppressive drugs with their debilitating side effects, such as skin warts, cataracts, and increased risks of heart disease, diabetes, and serious infections. If the results are borne out in a larger group of patients, the Mass. General technique has the potential to help transplant recipients live longer. Within 10 years, half of all transplanted organs fail because of chronic rejection, a bleak predicament in this era of organ shortages.
"This is landmark work," said Dr. Joshua Miller, an organ transplant researcher at Northwestern University's Feinberg School of Medicine in Chicago.
Other researchers cautioned that only the healthiest patients may be able to endure the rigorous treatments, including chemotherapy and radiation, that precede the transplant. Continued...

Kidney Racket

2008-01-29T09:10:00.000-05:00

Kidney racket: 'Nothing against two who left country'Times of India, India - 5 hours ago"Medical investigation of another person shows that his kidney can't be transplanted. So we had nothing to stop them from leaving. But they have promised to ...
Kidney racket: NCR labs, docs suspect Times of India
Police trace more hospitals linked to kidney racket
SifyHunt for 'Dr Horror' after police close clinic in kidney swaps raid
Times OnlineHindu - Hindustan Times all 102 news articles »

The Global Kidney RacketWired News - Jan 28, 2008"Inside, it’sa state-of-the-art hospital that is at the centre of a global kidney racket uncovered in police raids through Thursday night and Friday. ...

Northwestern Memorial trial may wean kidney transplant patients off antirejection drugs

2008-01-28T09:18:00.000-05:00

Science Centric— 25 January 2008 07:43 GMT

After a transplant surgery, anti-rejection drugs for the organ recipient are a must, but with prolonged use can have serious side effects, including infections, heart disease and cancer. A team led by Joshua Miller, MD, a researcher at Northwestern University’s Feinberg School of Medicine, is working with Northwestern Memorial Hospital’s department of organ transplantation to enrol qualifying subjects in a new research study that seeks to transplant stem cells from a kidney donor’s bone marrow into the recipient, with the hope of gradually eliminating the need for anti-rejection drugs. If research proves successful, it would mean a dramatic change in the post-transplant quality of life for the transplant recipient.
Northwestern is the only centre in Chicago and one of four centres nationally looking at this topic. The Feinberg School of Medicine has received a four-year, $2.5 million grant from the National Institutes of Health to enrol 20 patients in the study, which is called ‘Donor Stem Cells, Campath, T/B Cell Regulation In HLA-Identical Renal Transplants.’
The first subjects to participate in the study underwent kidney transplant surgery on Thursday, Jan. 10. Sharon Flood of Pingree Grove, Ill. donated her kidney to her brother Steven Yelk of Gurnee, Ill., who suffers from polycystic kidney disease (PKD), which causes cysts filled with fluid to form throughout the kidneys. Eventually, these cysts take over the healthy kidney tissue and the kidneys fail. ‘Our family is very close and there are seven brothers and sisters, I was thrilled to learn that I was a match and would be able to help Steven,’ Sharon commented before the surgery.
Joseph Leventhal, MD, PhD, transplant surgeon, associate professor of surgery and director of the Living Donor Renal Transplant Program at Northwestern University’s Feinberg School of Medicine, preformed the kidney donor’s surgery and Michael Abecassis, MD, MBA, chief of the division of transplantation, and dean of clinical affairs for Northwestern University’s Feinberg School of Medicine, performed the recipient’s surgery.
‘The surgery was successful, everything went according to plan and the new kidney is functioning well,’ said Dr Abecassis. From here, the kidney recipient will begin the experimental portion of the study.
This study is open to HLA-identical sibling kidney donor and recipient pairs. HLA, or human leukocyte antigen, is one of a group of proteins found on the surface of white blood cells and other cells that play an important part in the body’s immune response to foreign substances. These antigens vary from person to person, and an HLA compatibility test is performed before organ transplantation to find out if tissues match between a donor and a recipient.
The study is limited to only HLA-identical sibling pairs because these siblings genetically have a more similar set of immunologic markers than a non-related HLA-identical pair. Because this population has the closest genetic relationship, they have the best chance for success with the study. Overall, HLA-identical siblings have very low rejection rates for kidney transplants but until now have still required immunosuppressive drugs to be taken for life.
How does it work?
Stem cells are formed at the marrow and are common blood cells from which other specialised blood cells, like immune cells, develop. These stem cells are considered important to help prevent rejection of the kidney transplant. By transplanting these cells from the kidney donor into the recipient, the study seeks to prove that the stem cells will mature in the recipient’s body and will allow his immune system to accept the new organ as his own.
For the kidney donor, the laparoscopic surgery occurs in the standard manner. After the kidney is removed, bone marrow is drawn from the donor’s hip bone. About three months following the surgery, the donor undergoes two procedures called leukopheresis, happening one day apart, where stem cells mobilised from the marrow are collected so that they can be given to the kidney recipient to help his body acclimate to the transplant.
Approximately one month before the transplant surgery, the recipient undergoes leukopheresis to draw white blood cells which are stored in a lab for later testing. After transplant surgery, the recipient receives four separate infusions of donor stem cells.
The stem cells are infused into the transplant recipient via an IV in a procedure that lasts about 15 minutes. The first infusion is five days after surgery, the next is about three months after surgery, then six months and finally nine months after the transplant. During this time the recipient is treated with Campath-1H, a potent antibody used extensively at Northwestern to prevent rejection, in addition to the other standard anti-rejection medications. About a year after the surgery, the subject is weaned off of one anti-rejection drug, then another. There are also ongoing tests to ensure the recipient is tolerating the kidney.
‘This is an exciting area of research which holds a great deal of promise if successful,’ says Dr Abecassis. ‘We are excited to be the only centre in the region offering this to qualifying patients.’
Source: Northwestern Memorial Hospital

Kidney Headlines PKD Blog

2008-01-26T10:52:00.000-05:00

Kidney And Liver Cancer Drug Raises High Blood Pressure Risk
Written by Catharine Paddock
Sorafenib, a new anti tumour (antineoplastic) drug marketed by Bayer under the brand Nexavar, and used to treat patients with advanced kidney or liver cancer, has been found to increase significantly the risk of developing high blood pressure...[read article]

Beyond The Abstract - Pathological Evidence Of Necrosis In Recurrent Renal Mass Following Treatment With Sunitinib

Low Dose Computed Tomography For The Evaluation Of Flank Pain In The Pregnant Population

Recipient Got Wrong Donor Kidney And Had To Have It Removed

Kidney Cysts: Not All Created Equal

Beyond The Abstract - Sequential Bilateral Minimum Incision Endoscopic Radical Nephrectomy In Dialysis Patients With Bilateral Renal Cell Carcinomas

Beyond The Abstract - The Value Of Combined Use Of Survivin, Cytokeratin 20 And Mucin 7 MRNA For Bladder Cancer Detection In Voided Urine

Overlap Of Voiding Symptoms, Storage Symptoms And Pain In Men And Women

The show goes on for Steven (Cojo) Cojocaru

2008-01-26T10:50:00.000-05:00

BY PATRICK HUGUENIN
Thursday, January 24th 2008, 4:00 AM

Steven (Cojo) Cojocaru has his hands on the latest must-have accessory. And it's not from Dior Homme.
In 2004, the over-the-top, celebrity-sniping, red-carpet TV fashion critic stepped away from his cameras at "Entertainment Tonight" to battle polycystic kidney disease (PKD), a genetic condition that threatened his life.
Lucky for Cojocaru, he got a healthy replacement, something both hard to find and, he says, less often discussed than its vital cousins, the heart, lungs and liver.
"Kidneys are under the radar," he says. "They're not A-list organs. Hearts are hot. Hearts are in. Kidneys are out. I want to make kidneys as hot as a Balenciaga handbag."
Cojocaru's mission of awareness starts with his second autobiographical book, "Glamour, Interrupted: How I Became the Best-Dressed Patient in Hollywood," out Tuesday.
Steven (Cojo) Cojocaru has his hands on the latest must-have accessory. And it's not from Dior Homme.
In 2004, the over-the-top, celebrity-sniping, red-carpet TV fashion critic stepped away from his cameras at "Entertainment Tonight" to battle polycystic kidney disease (PKD), a genetic condition that threatened his life.
Lucky for Cojocaru, he got a healthy replacement, something both hard to find and, he says, less often discussed than its vital cousins, the heart, lungs and liver.
"Kidneys are under the radar," he says. "They're not A-list organs. Hearts are hot. Hearts are in. Kidneys are out. I want to make kidneys as hot as a Balenciaga handbag."
Cojocaru's mission of awareness starts with his second autobiographical book, "Glamour, Interrupted: How I Became the Best-Dressed Patient in Hollywood," out Tuesday.
Read More

Breakthrough in Transplants

2008-01-24T10:43:00.000-05:00

Scientist triumphs after setback in kidney transplant method
Boston Globe, United States - 7 hours ago
Then in October 2003, Andrews, a software engineer with polycystic kidney disease, went in for his experimental procedure. When the surgery was complete, ...Some transplant patients OK without years of drug treatment Chicago Tribune

all 382 news articles »

Kidney Transplants Without Lifetime On Immunosuppressive Drugs In Sight

Combined Organ And Bone Marrow Transplant Allows Patients To Halt Immunosuppression

AAKP 2008 Kidney Beginnings: Live Schedule Announced

2008-01-23T11:38:00.000-05:00

Main Category: Urology / Nephrology
Article Date: 23 Jan 2008 - 3:00 PST
The American Association of Kidney Patients (AAKP) is pleased to release its 2008 Kidney Beginnings: Live program schedule. Kidney Beginnings: Live is one of AAKP's most popular programs. This FREE educational seminar targets those recently diagnosed with chronic kidney disease (CKD), those at risk of developing CKD and their family members. CKD is the gradual loss of one's kidney function over time. Diabetes, hypertension and family history of reduced kidney function are three of the main causes of kidney disease. Kidney Beginnings: Live teaches individuals about kidney function, how diabetes and hypertension can further damage the kidneys, diet management and more. AAKP will host 12 Kidney Beginnings: Live programs this year in cities across the United States including Atlanta, Ga., West Palm Beach, Fla., Chicago, Ill., Washington, D.C., Detroit, Mich., Houston, Texas, Denver, Colo., San Diego, Calif. and Baltimore, Md. The first program is scheduled for Feb. 23, at the Hyatt Regency Suites Atlanta Northwest in Marietta, Ga., from 9 a.m. - 12 p.m. Patients can register for any of the programs online at http://www.aakp.org, by clicking on the "Educational Programs & Events" button, or by calling AAKP at (800) 749-AAKP. A complete list of program dates and locations are posted on the Web site. "AAKP is proud to work with Ortho Biotech Products, L.P. to bring patients this program," said Kris Robinson, AAKP Executive Director/CEO. "Patients walk-away feeling more knowledgeable about their disease and empowered to take ownership of their healthcare."
AAKP is the voluntary, patient organization, which for more than 35 years, has been dedicated to improving the lives of fellow kidney patients and their families by helping them deal with the physical, emotional and social impact of kidney disease. The programs offered by AAKP inform and inspire patients and their families to better understand their condition, adjust more readily to their circumstances, and assume more normal, productive lives in their communities. American Association of Kidney Patients

Cilia link seeing and peeing

2008-01-22T06:26:00.000-05:00

Comment on this blog

I've officially heard my favorite one-liner here at the Keystone symposium on the molecular basis for biological membrane organization. In her presentation on the molecular link between polycystic defects such as retinopathies and polycystic kidney disease, Angela Wandinger-Ness of the University of New Mexico offered this gem: "There is a connection between seeing and peeing." After the giggles subsided, Wandinger-Ness went on to describe her research on the commonality of primary cilia malfunction in such diseases. She said that problems with the localization of signaling proteins to the ciliary membranes and the subsequently disrupted membrane trafficking may be the key to problems with kidney function, vision, and other sensory pathways. In vision, for example, mutations in the ciliary protein rhodopsin - which functions in initiating light sensing and photoreceptor formation - may lead to developmental disorders resulting in cell death and degeneration of the retina. Mutations in polycystic kidney disease genes, such as PKD1, prevent localization of their corresponding membrane proteins - which normally sense urine flow in urinary collecting ducts and serve as calcium channels - to cilia in the kidney and disrupt normal kidney development and function. She also identified a common amino acid motif that seems essential to the normal localization and function of ciliary proteins in everything from olfaction to retinal function. "The primary cilium is the unifying link," she said.

Kidney Headlines PKD Blog

2008-01-18T08:03:00.000-05:00

Novadaq's SPY System Receives Clearance For Use In Organ Transplant Surgery

Fifty Per Cent Increase In Organ Donation Possible Within Five Years, UK

PKD Blog Medical Headlines

2008-01-14T07:38:00.000-05:00

British PM Opens Debate On Presumed Consent Organ Donation
Written by Catharine Paddock
British Prime Minister Gordon Brown wrote in the Sunday Telegraph yesterday that the UK's organ donor system is in need of an overhaul, and introduced the idea that perhaps it should be based on presumed consent, where everyone is automatically a donor, and when they die their organs are presumed to be available for donation,...[read article]

Organ ruling hits home
ChronicleHerald.ca, Canada - Jan 12, 2008(CP) David Watson has polycystic kidney disease and may well be in need of a kidney transplant one day. Health Canada’s recent decision to exclude sexually ...

Fresenius Medical Care Selected To Provide Dialysis Care To More Than 400 Patients In The U.K.

Causes and Risk Factors of Polycystic Kidney Disease

2008-01-10T08:31:00.000-05:00

Causes and Risk Factors of Polycystic Kidney Disease
This disease appears to occur all over the world among all socioeconomic and ethnic groups. Men and women are affected equally, and about 500,000 Americans have PKD.
Autosomal dominant PKD is the most common inherited disease in the United States. People get the disease from a parent who has PKD. If one parent has autosomal dominant PKD, each child has a 50/50 chance of inheriting the disease. In autosomal recessive PKD, parents may have no symptoms but still carry a recessive gene for the disease. If both parents have this recessive gene, one-fourth of the children can inherit the disease.

Symptoms of Polycystic Kidney Disease
PKD usually affects both kidneys. The symptoms include abdominal or flank pain, blood in the urine (caused by blood vessels breaking in the cysts), kidney stones, and recurring bladder or kidney infections. High blood pressure is very common, occurring in about 50 percent of all people who have the disease. However, not everyone who has one of more of these symptoms has PKD. A high proportion of PKD patients develop kidney failure, which may require dialysis treatments or a kidney transplant.

Diagnosis of Polycystic Kidney Disease
In addition to a medical history and physical exam, your physician may order blood tests and a urinalysis (urine test). Ultrasonography, which uses sound waves, is sensitive enough to detect most cases of PKD. Computed tomography (CT scan), especially when combined with dye infusion, is one of the most sensitive tests available.

Treatment of Polycystic Kidney Disease
At present, there is no specific treatment for PKD. However, it is important for anyone with PKD to have regular checkups.
Treatment is confined to complications such as infection, stones, bleeding and hypertension.
A low-protein diet may slow progression of the disease.
Operations, such as cyst puncture or removal, designed to relieve pressure, may make the condition worse.
Blood pressure control and prevention of kidney stones and infections have improved the prognosis for those with PKD. Dialysis and transplantation are other alternatives.

Questions To Ask Your Doctor About Polycystic Kidney Disease
What tests will be done?
Are there risks or side effects associated with these tests?
How serious is this condition?
Has this condition affected any other vital organs?
What type of treatment will you be recommending?
How effective is this treatment?
Are there any alternative treatments?
Will you be prescribing any medication?What are the side effects?

Source
http://www.healthscout.com/ency/68/69/main.html

Multiple Renal Cysts, Urinary Concentration Defects, and Pulmonary Emphysematous Changes in Mice Lacking TAZ.

2008-01-09T07:31:00.000-05:00

Makita R, Uchijima Y, Nishiyama K, Amano T, Chen Q, Takeuchi T, Mitani A, Nagase T, Yatomi Y, Aburatani H, Nakagawa O, Small EV, Cobo-Stark P, Igarashi P, Murakami M, Tominaga J, Sato T, Asano T, Kurihara Y, Kurihara H.
Department of Physiological Chemistry and Metabolism, The University of Tokyo, Graduate School of Medicine, Tokyo, Japan; Department of Developmental Medical Technology (Sankyo The University of Tokyo, Graduate School of Medicine, Tokyo, Japan.
TAZ (transcriptional coactivator with PDZ-binding motif), also called WWTR1 (WW domain containing transcription regulator 1), is a 14-3-3-binding molecule homologous to Yes-associated protein (YAP). TAZ acts as a coactivator for several transcription factors as well as a modulator of membrane-associated PDZ domain-containing proteins, but its (patho)physiological roles remain unknown. Here we show that gene inactivation of TAZ in mice resulted in pathological changes in the kidney and lung that resemble the common human diseases, polycystic kidney disease and pulmonary emphysema. Taz-null/lacZ knock-in mutant homozygotes demonstrated renal cyst formation as early as embryonic day 15.5 with dilatation of Bowman's capsules and proximal tubules, followed by pelvic dilatation and hydronephrosis. After birth, only one-fifth of TAZ-deficient homozygotes grew to adulthood and demonstrated multicystic kidneys with severe urinary concentrating defects and polyuria. Furthermore, adult TAZ-deficient homozygotes exhibited diffuse emphysematous changes in the lung. Thus, TAZ is essential for developmental mechanisms involved in kidney and lung organogenesis, whose disturbance may lead to the pathogenesis of common human diseases. Key words: Transcriptional coactivator, Concentration defect, Polycystic kidney disease, Kidney developmetn, Pulmonary emphysema.
PMID: 18172001 [PubMed - as supplied by publisher]

Pretransplant laparoscopic nephrectomy in adult polycystic kidney disease: a single centre experience.

2008-01-03T08:22:00.001-05:00

BJU Int. 2008 Jan;101(1):94-7. Epub 2007 Oct 8.
Desai MR, Nandkishore SK, Ganpule A, Thimmegowda M.
Department of Urology, Muljibhai Patel Urological Hospital, Nadiad, Nadiad Gujarat, India. mrdesai@mpuh.org
OBJECTIVE: To report our experience with pretransplant laparoscopic nephrectomy in patients with autosomal dominant polycystic kidney disease (ADPKD), as ADPKD often progresses to end-stage renal disease and most azotaemic patients with ADPKD have enlarged kidneys, making graft placement difficult. MATERIAL AND METHODS: We retrospectively reviewed the medical records of 13 patients with renal failure attributable to ADPKD who underwent pretransplant laparoscopic nephrectomy (21 renal units) from August 2002 to December 2006. Five patients had a unilateral nephrectomy, seven had a staged bilateral nephrectomy, and one had a simultaneous bilateral nephrectomy. All patients underwent subsequent living-related renal transplantation. The operative duration, haemoglobin decrease, blood transfusion, hospital stay, analgesic requirement and time to receipt of a transplant were compared with those of patients who underwent open pretransplant nephrectomy (14 patients) from 1984 to 2001. RESULTS: Kidneys of a size to interfere with graft placement were the commonest indication for surgery (eight patients). In comparison with open surgery, the mean (SD) hospital stay at 9.26 (2.9) vs 4.86 (0.9) days, analgesic requirement at 320 (120) vs 221 (120.5) mg of tramadol, blood transfusion rate at 1.3 (0.5) vs 0.9 (0.6) units, period to receive a graft kidney at 29.77 (4.6) vs 9.14 (3.38) days, were significantly less with laparoscopy. The complications noted were single instances of splenic capsular tear, pleural tear, sub-acute intestinal obstruction and vena caval injury. CONCLUSION: Pretransplant laparoscopic nephrectomy in patients with ADPKD has all the benefits of minimally invasive surgery such as reduced intraoperative blood loss and minimal postoperative pain leading to early and faster convalescence. These benefits help in decreasing the period between nephrectomy and transplantation. The surgeon needs to have considerable experience in laparoscopy before embarking on laparoscopic pretransplant nephrectomy.
PMID: 17922857 [PubMed - in process]

Molecular Basis of Autosomal Recessive Polycystic Kidney Disease (ARPKD).

2008-01-01T11:34:00.000-05:00

Adv Anat Pathol. 2008 Jan;15(1):54-58.
Links
Molecular Basis of Autosomal Recessive Polycystic Kidney Disease (ARPKD).
Al-Bhalal L, Akhtar M.
*Department of Pathology and Laboratory Medicine, King Khalid University Hospital Riyadh, Saudi Arabia †Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY.
Autosomal recessive polycystic kidney disease (ARPKD) is a serious genetic disease characterized by cystic changes in the collecting ducts of the kidney and bile ducts within the liver. The gene for ARPKD (PKHD1) is located on chromosome 6p12 and encodes a protein called fibrocystin/polyductin (FPC), 1 of many proteins that are normally present at the primary cilia of the renal tubules and intrahepatic bile ducts. The severity of the clinical disease depends on the type of genetic mutations. Although exact function of FPC is not fully known, it is generally felt that like many of the other ciliary proteins, it plays a vital role in maintaining the structural integrity of organs such as kidney and liver, by modulating important cellular functions, including proliferation, secretion, apoptosis, and terminal differentiation. FPC probably works in conjunction with cellular proteins involved in autosomal dominant polycystic kidney disease that is, polycystin-1 and polycystin-2, which are also located in the primary cilia. Genetic abnormalities in PKHD1 may result in structural and functional abnormalities of FPC, leading to cystic phenotype.
PMID: 18156813 [PubMed - as supplied by publisher]

PKD Blog Kidney Headlines

2007-12-31T09:53:00.000-05:00

Comparative Results Of Shockwave Lithotripsy For Renal Calculi In Upper, Middle, And Lower Calices

Bladder Substitution By Ileal Neobladder For Women With Interstitial Cystitis

A New Treatment Option For Patients With Renal Cancer

AMAG Pharmaceuticals, Inc. Submits New Drug Application To FDA For Ferumoxytol In Chronic Kidney Disease Patients

In Breakdown Of Kidney Filtration Receptor Protein Appears To Be Key

Prestigious Medical Journal Publishes Data On Xcorporeal's Wearable Artificial Kidney

Kidney Donor Evaluation Detects Aneurysm

Researchers Discover Link Between Chronic Kidney Disease And Oxygen Deprived Tissue

Oncologic Outcomes Of Extravesical Stapling Of Distal Ureter In Laparoscopic Nephroureterectomy

Study Questions Impact Of Hemoglobin Variations On Mortality In Dialysis Patients

Transplant costs

2007-12-30T07:07:00.000-05:00

A transplant costs, on average, about $105,000 , though price varies by case. Private insurers cover the transplants to varying degrees. The program isn’t yet certified by Medicare, and until that happens, it’s expected that only some of the private insurance companies will provide the maximum benefit. Medicare is expected to make a site visit to consider certification of the program – a precursor to coverage by the governmental insurance program – in the next few months.

http://www.journalgazette.net/apps/pbcs.dll/article?AID=/20071230/FEAT/712300418

Bill to close legal loophole in paired kidney donations passes House, Senate

2007-12-29T06:54:00.000-05:00

PKD Foundation supports legislation, but treatment or cure to avoid transplant is ultimate goal

(Washington, DC) December 11, 2007—A bill amending the National Organ Transplant Act to make paired kidney donations easier has passed the U.S. House and Senate. The Living Kidney Organ Donation Clarification Act (S. 487/H.R. 710) will benefit more than 600,000 Americans living with PKD.
Many PKD patients find friends or family members willing to donate a kidney. But often, they are not compatible match for the patient they hope to help. Instead, hospitals find other families with willing donors and swap kidneys between the two patients.

H.R. 710 clears up any legal questions about those specific types of kidney donations; by indicating that transfer of paired kidney donations would not be considered something that was done for financial gain. This legislation also will allow the Organ Procurement and Transplant Network to move quickly to establish a national registry of pairs which transplant centers can begin to implement. “We applaud the Congress for recognizing the life-saving benefits of paired organ donations,” said Dan Larson, President and CEO of the PKD Foundation. “A treatment or cure for polycystic kidney disease (PKD) would eliminate the need for kidney transplants for 600,000 Americans who suffer from PKD,” he added. “But until then, closing this legal loophole will undoubtedly increase the number of kidneys available for transplantation.”

The Senate version of this legislation (S. 487) was sponsored by Sen. Carl Levin (D-MI). The House version was sponsored by Rep. Charlie Norwood (R-GA) , who passed away earlier this year. President Bush is expected to sign the bill into law.

Source: The PKD Foundation

Polycystic kidneys: a cautionary story.

2007-12-28T05:32:00.000-05:00

Currie RJ, Freeman SJ, McCormick F, McGonigle RJ.
Department of Radiology, Derriford Hospital, Plymouth PL6 8DH, UK.
We describe the imaging appearances of a patient with bilateral, synchronous, multiloculated renal cell carcinoma with a predominantly cystic nature. The patient had progressive chronic renal failure. He was initially erroneously diagnosed as having autosomal dominant polycystic kidney disease (ADPKD) on the basis of the imaging findings. We believe this to be the first report describing bilateral synchronous renal carcinomas replacing the renal parenchyma imitating ADPKD.
PMID: 18065639 [PubMed - in process]

See 'SiCKO' for Free:

2007-12-27T08:34:00.000-05:00

TODAY at 7:00 PM in Asheville, North Carolina
December 28th at 6:30 PM in Hayward, Wisconsin
December 29th at 2:00 PM in Bonham, Texas
December 30th at 7:00 PM in Asheville, NC
January 5th, Vaughan, Ontario, Canada
January 7th at 5:45 PM in Spring Hill, Florida
January 7th at 6 PM, Hilton Head Island, SC
January 10th at 6:30 PM in Stamford, Connecticut
January 11th at 7 PM in Stillwater, Oklahoma
January 29th All Day Long in Salt Lake City, Utah

Polycystic Kidney Disease Spreading the word

2007-12-27T08:26:00.000-05:00

BRENT DAVIS, RECORD STAFF
Kitchener resident Nina Young is living with polycystic kidney disease and is trying to raise more awareness about the genetic illness.

('Email story');

It is a disease which can swell the kidneys from the size of a human fist to the size of a football, weighing as much as 38 pounds each. It riddles them with painful, fluid filled cysts, which grow as big as baseballs, crowding out normal kidney tissue.

The culprit is polycystic kidney disease, one of the most common of all life-threatening genetic diseases. By age 60, half of those with the dominant form of the disease experience kidney failure and require a kidney transplant or dialysis to keep them alive.
Those with the disease also face a higher risk of heart problems, stroke, brain aneurysms and cysts in other areas of the body, such as the liver.
There are more than 63,000 people in Canada and 12.5 million people worldwide with the disease. There is no treatment and no cure, although three drugs are being tested which could slow the development of cysts.
Nina Young, 26, of Kitchener, learned she had the disease when she was just 13. It has cut a wide swath through her family.
Her grandfather died from its complications as he was preparing to begin dialysis. Her mother Laura, who lived in Kitchener, succumbed in the summer of 2006 at age 45.
Of her mother's siblings, six have the disease and one does not. Another died in infancy of unknown causes.
Two have died as adults and two have had successful kidney transplants. Young's brother and several cousins also have the disease.
After eight troubled years on dialysis, Young's mother had climbed near the top of the transplant waiting list before her death.
Although Young's own kidneys and heart are currently fine, she is already having problems with her blood pressure and has a number of cysts on her kidneys and liver.
A single mother of an eight-year-old, she is unable to work outside the home and provides home day care.
"It's not an easy feeling knowing that I may have 10 years left until I'm on dialysis," Young says in a recent interview at her home.
But she is trying to stay positive.
Young is on a mission to educate people about polycystic kidney disease, hoping that awareness will prompt more research into treatments and possibly a cure. She is involved with the Polycystic Research Society of Canada as a volunteer representative for Waterloo Region, which does not have a chapter. The society has support groups and holds an annual walk to aid in funding research.
Young is moving to her native Newfoundland next summer to be closer to her family and plans to start a chapter there. She has a blog which details her health struggles. (www.pkdfighter-ninasblog.blogspot.com.)
In one poignant entry she writes: "watching my family, and especially my mom, fight so hard to just live is what has given me the courage to stand up and make a difference.
"I will continue fighting for them, for myself and for every other person out there in the world who is affected by this disease. I will not give up until there is a cure."
Young's determination is a departure from the depression she experienced while growing up.
Every time the phone rang, it seemed another family member was seriously ill. Depression often accompanies the disease.
"It's a very emotional thing.," she says. "There was a time, I couldn't talk about it at all. I'd just break down and cry."
She understands now that constant worry is counter-productive.
"Stress is terrible on your body, because it causes hypertension (high blood pressure). Cysts don't like that. It aggravates them and they start growing even more."
On the advice of a renal dietitian, she eats a low-protein, vegetarian, soy-based diet aimed at slowing the formation of cysts.
Lorrie Rome, national director of scientific programs for the Missouri-based PKD Foundation, says one of the drugs being tested is particularly promising.
"Probably within five to six years, if the clinical trials hold up, it should be on the market," Rome predicts.
"PKD research is a very exciting, dynamic and potentially therapeutically promising field," said Rome.
Young's eagerness to promote awareness and research is partly fuelled by her desire to ensure her daughter, Laura, has a better future, should she develop the disease.
When Young learned she was pregnant at age 18, "it was the greatest moment of my life. Now I have somebody here to go on for," she recalled thinking.
But Young feels the loss of her mother deeply. She cared for her during her horrible ordeal.
Her kidneys needed to be removed when they ballooned to 11 pounds and 13 pounds each.
As cysts grow, they can rupture and bleed, causing infection.
She required several surgeries to find a site that could withstand the catheter needed for dialysis.
Her final option was peritoneal dialysis, with a catheter running into her belly. But gangrene set in at the opening created for the catheter. The wound would not heal and she died not long afterward.
Young is encouraged by the research underway and is determined to stay as well as possible until there is a breakthrough.
The disease can be diagnosed through tests such as ultrasound, CT (computed tomography) scan and MRI (magnetic resonance imaging) scan.
Genetic testing is also available, but there are pros and cons with that, notes Rome.
In the United States, some people have been denied medical and life insurance based on their genetic testing results.
Young has not been able to get life insurance because of her illness. But, despite the many challenges that come with the disease, she tries to be upbeat.
"It's something you just have to learn to live with and do the best you can," she says.
akelly@therecord.com
WHAT IS IT?
Polycystic kidney disease (PKD), the most common of all life-threatening genetic diseases, affects more people than Down syndrome, cystic fibrosis, muscular dystrophy, hemophilia, sickle cell anemia and Huntingdon's disease combined.
It comes in two hereditary forms. They are:
1. Autosomal dominant, which affects one in 150 people worldwide. Parents with the dominant form of the disease have a 50 per cent chance of passing it on to each of their children.
2. Autosomal recessive, which affects one in 20,000 babies and often leads to death in their first year of life. Parents who carry the gene for the recessive form have a 25 per cent chance of passing the disease to each of their children.
The dominant form has two types of genes, known as PKD 1 and PKD2. Eighty-five per cent with the dominant form have the PKD 1 gene, which leads to more aggressive disease. The disease is also more aggressive in men and those who develop high blood pressure in their early 20s.
SOURCE: PKD FOUNDATION
SYMPTOMS
high blood pressure occurs in 50 per cent of patients
constant or intermittent pain in the back and the side of the stomach
blood in the urine
kidney stones
frequent urinary tract infections
heart problems
brain aneurysms
stroke
ON THE WEB
www.pkdcure.org
www.geocities.com/walkforpkdtoronto
www.mayoclinic.com
SOURCES: POLYCYSTIC KIDNEY RESEARCH SOCIETY OF CANADA, PKD FOUNDATION

http://news.therecord.com/Life/article/285590

Analysis: 'Sicko' numbers mostly accurate; more context needed

2007-07-01T09:21:00.000-04:00

By A. Chris GajilanCNN
(CNN) -- Michael Moore's "Sicko," which opened nationwide Friday, is filled with horror stories of people who are deprived of medical service because they can't afford it or haven't been able to navigate the murky waters of managed care in the United States.
It compares American health care with the universal coverage systems in Canada, France, the United Kingdom and Cuba.
Moore covers a lot of ground. Our team investigated some of the claims put forth in his film. We found that his numbers were mostly right, but his arguments could use a little more context. As we dug deep to uncover the numbers, we found surprisingly few inaccuracies in the film. In fact, most pundits or health-care experts we spoke to spent more time on errors of omission rather than disputing the actual claims in the film.
Whether it's dollars spent, group coverage or Medicaid income cutoffs, health care goes hand in hand with numbers. Moore opens his film by giving these statistics, "Fifty million uninsured Americans ... 18,000 people die because they are uninsured."
For the most part, that's true. The latest numbers from the Centers for Disease Control and Prevention say 43.6 million, or about 15 percent of Americans, were uninsured in 2006. For the past five years, the overall count has fluctuated between 41 million and 44 million people. According to the Institute of Medicine, 18,000 people do die each year mainly because they are less likely to receive screening and preventive care for chronic diseases.
Moore says that the U.S. spends more of its gross domestic product on health care than any other country.
READ MORE

Autopsy report ~ Edith Isabel Rodriguez suffered " Adhesion Related Disorder!"

2007-06-30T16:00:00.001-04:00

Edith Isabel Rodriguez suffered " Adhesion Related Disorder!" A contributory if not THE end means disease of which she died!

Edith Isabel Rodriguez was a victim of "Adhesion Related Disorder," just as IHRT suspected and predicted.
This prediction was something that no medical "professional" was able to predict, suspect and most disturbing to IHRT, was not able to diagnose properly!

Edith presented to the ER a number of times over a short period of time, "was called a "frequent flyer" prescribed analgesics for pain, miss-diagnosed due to the lack of knowledge of ARD, and worse, lack of medical intervention, inhumane treatment and ultimately met her death lying on the floor in the waiting area of Martin Luther King Hospital in LA, with a janitor cleaning around her pain riddled body as loved ones and other patients watched in disbelief!

The sad truth is that hundreds, maybe thousands of persons afflicted with ARD are receiving this very same "lack of treatment" in ER's all over the USA....and if this med student web site is any indication of the caliber of "Dr.'s" who are going to fill these ER's, person afflicted with ARD face this same type of death without dignity or proper medical intervention, just as Edith did!

Read the Adhesion Quilt for stories very similar to Edith's as each person pleads for help from one of the most painful conditions imaginable. ARD patients can be "frequent flyers" to E.R.. It's actually a common phrase in an adhesion sufferer's story.

Not only was Edith's death a tragedy, it appears that her autopsy was just as "sloppy" and "crude" as her death at the hands of "medical professionals!" Her autopsy report is filled with errors and inconsistencies as the hands of those in the corner's office of LA who did the "investigation" & "autopsy!" Would this have happened if "Edith I. Rodriguez" was "Anna Nicole Smith?"

Edith Isabel Rodriguez seems to have been treated as a "Jane Doe" at the coroner's office.

.........Until you know what hit the fan.

BOTH these ladies seemed to have a history of drug taking, with "Anna Nicole Smith" appearing to be the worst of the two, both died young, and both were taking prescription medication at the time of their deaths..and that is where the similarities seem to end!
IHRT called it correctly, and NOT one medical person was able to do that, and we did it without the autopsy results! We will say that, "WE told you so!"

Edith Isabel Rodriguez "Adhesion Related Disorder"

Post-surgical intra-abdominal adhesions

Date of birth: 2/1/1964

Date of death: 5/9/2007

Place of death: Martin Lutheran King - LA

Pg. 1 Synopsis: History of "illicit narcotic" abuse" no mention of an "Iatrogenic" disorder!

Pg. 2 In dormant/witness statement: Diagnostic tests results - Negative for abnormal pathology

Autopsy exam:

Pg. 1 Anatomical summary: D - Lower abdominal and pelvic regions with adhesions.

Pg. 2 NO tracking from illicit drugs..(IHRT asks:"so just how bad was the "Illicit drug taking?")

Pg. 3 Evidence of "old surgery" scar at middle lower portion of the abdomen midline just under the umbilicus is vertically oriented and measures 7.5 inches. (Laporotomy)

Pg. 4 Prior Appendectomy - Extensive adhesions in the lower abdominal quadrant! (IHRT adds that THIS is a VERY painful condition!)

Edith's autopsy report states that she died after "collapsing in the ER" and "not being able to be resuscitated," no mention that Edith lay bleeding and withering in pain on the floor of the ER in full view of the ER staff!
Edith's autopsy reports gives her age as both 43 years of age, AND 53 years of age! Edith's autopsy report states that she did not have any bowel strangulation, but adhesions most certainly narrow the intestinal passages and constricts constipated stool!

One x-ray could have seen the mega colon and thus her life could have been saved.

Was she ignored because this E.R suspected she had adhesions and also needed emergency surgery.
Adhesions are usually a surgeons worst nightmare!
Adhesions are can be dangerous to lyse. Adhesiolysis can be very time consuming thus offers a medical facility no profits.
Most surgeons are pretty nervous about their medical malpractice rates.

IHRT suspects that many are turned away and discriminated against just for having prior surgeries or if the word adhesions is on any post op report.
IHRT says very possible!

Edith's autopsy report states her death was an "accidental!"

Edith Isabel Rodriguez is, sadly, a prime example of what persons afflicted with ARD face when seeking medical intervention for their pain and various symptoms!

Edith's death was NOT due to diabetes, hypertension, overweight, nor gender, race, being rich or poor, having a criminal record or not, drug addiction, being transient in nature, being a mother, a grandmother, a friend, a sister, an aunt, a person....Edith died because she had, "Adhesion Related Disorder" and this IS how persons afflicted with ARD are treated by medical "professionals" in Emergency Rooms all across the USA!

IHRT predicts that this treatment is not likely to get better after reading the comments by "medical students" in the following link! Non of the med students had a clue as to what might have caused Edith's symptoms, and why she presented so often to the ER, nor why all the diagnostic tests were "normal!" IHRT knew the answer to ALL of those answers, and they was right!
Many adhesion sufferers immediately thought, " Edith IS one of us I bet" and now we have obtained the horrible truth of the matter. The autopsy confirmed our worse fears,

Read "Edith's Autopsy " report for yourself!

Edith Isabel Rodriguez had severe abdominal adhesions.

Edith Isabel Rodriguez will save many lives we pray with her tragic posthumous story.

Adhesion sufferers should be forever armed at all times with our operative reports and Edith Rodriguez' autopsy report.

Firmly stand your ground.

You will be presenting to the likes of these medical professions in the future. Here is the link, "Student Doctor Network Forums"

LADoc00 writes:

"The lady was a drug addict and had warrants for her arrest. Why does anyone think this was unintentional?? Was she even a US citizen FFS? On the face of it, saving her would have been FAR more of a tragedy for America.LET THESE PEOPLE DIE. I cant stress this enough.I want to give MLK adminstrators a medal for this not my scorn.
__________________Where is the horse and the rider? Where is the horn that was blowing? They have passed like rain on the mountain, like a wind in the meadow; The days have gone down in the West behind the hills into shadow."

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Is he just kidding?? IHRT can't tell!

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

These are the facts, plain and simple..and this was "Manslaughter," plain and simple!

Sicko opens today

2007-06-29T10:20:00.001-04:00

Today is the Day for "Sicko"...a letter from Michael Moore

Movie Trailer

"Where can I see the film?"

TONIGHT at 9:00 PM ET:Check Out Mike on 'Larry King Live'

"Would you patent the sun?" -- Jonas Salk, developer of the polio vaccine

Outnumbered; Pharmaceutical giants might as well take a chill pill

What Do They Have to Lose?

The Rug Out from Under Their Feet

SICKO OPENS TODAY! EVERYWHERE!!

Kidney Notes PKD Blog

2007-06-27T10:31:00.000-04:00

American Association Of Kidney Patients Develops Home Dialysis Magazine

Roche's New Long-acting ESA May Almost Halve Time Healthcare Professionals Spend On Anaemia Management In Dialysis Centres Each Year

EDAP TMS S.A. Adds Global Distribution Of LMA StoneBreaker(TM) System

Radical Nephrectomy Is Associated With Increased Mortality In Patients With Small Renal Tumors

MRI Is Inadequate For Monitoring Renal Tumor Destruction Following Radio Frequency Ablation

Traveling can help cure medical costs

2007-06-27T10:29:00.000-04:00

TRACY CORREA
Fresno Bee

Three years ago, James Dodd of Hanford, Calif., weighed more than 400 pounds.
He had trouble breathing at night and doing work around his house. He was desperate for help.
But when Dodd, 54, started looking into lap-band weight-reduction surgery for relief, his insurance company denied coverage, calling the procedure "experimental."
An Internet search for alternatives turned up Bajanor Hospital in Tijuana, Mexico, where doctors perform the procedure for $7,200 -- less than the $37,000 he said he was quoted at the time.
He got the surgery and is happy with the results, despite serious complications.
"Everything in life is a risk," said Dodd, now recovered and slimmer. He said he also could have had complications in the United States, adding, "It would have bankrupted me here."
Dodd is among an increasing number of Americans venturing out of the country -- to places like Mexico, Thailand, the Philippines and India -- for medical treatment because of the high cost of health care.
Patients can save as much as 80 percent on procedures done by medical professionals often educated and trained in the United States at hospitals increasingly accredited for meeting U.S.-like standards.
An estimated 150,000 people traveled abroad last year for medical treatment, and the number is expected to double by 2010, said Josef Woodman, author of "Patients Beyond Borders: Everybody's Guide to Affordable, World-class Medical Tourism." Nearly half had medically necessary surgeries, such as hip replacements or spinal work, heart surgeries, even cancer treatment.
The book, released in March, tells how patients can save 25 percent to 75 percent on anything from LASIK eye repair to neurosurgery by traveling outside the United States.
Health-industry representatives said U.S. health-care costs more, in part, because of skyrocketing medical-malpractice insurance and the higher wages and benefits paid to hospital workers.
Costs are high, said Woodman in a telephone interview, "because Americans demand from cradle to grave, the most expensive treatment, the most extensive testing."
He said the American health-care system is "stuck" because insurance companies are dictating what can and can't be covered, and consumers are unable to negotiate direct payment to providers.
Dr. Steven Parks, a longtime surgeon and clinical professor for the University of California-San Francisco's Fresno-based medical-education program, said that while he has been all over the world and knows there is great medical care available, he advises caution.
He said there are also plenty of Third World countries with hospitals and doctors that don't meet U.S. guidelines and restrictions but offer huge discounts. Hospitals here have to meet certain standards, he said.
Those who choose to go abroad? "I think it is probably dangerous, and you are probably taking a risk with your life. I think you should find a way to get it done at the good hospitals in town," Parks said.
Woodman has traveled abroad for his own care. He went to Costa Rica for dental work -- a root canal, implants and follow-up care -- after looking at several other countries. He said he saved about $2,000.
The key to a good experience, he said, is to do your homework, find out about the doctors, try to interview them beforehand, and then ask about success rates and find out about the facility: "If they don't speak English, then move on."
Interest in traveling abroad for medical treatment has spawned a new industry: medical tourism. Companies are playing the role of travel agent and medical-care coordinator and linking American patients with overseas hospitals for a fee.
MedRetreat, based near Chicago, was one of the first when it started in 2003.
The company describes itself as "a medical gateway to health care abroad ... where smart medicine and exotic travel come together."
Company spokesman Patrick Marsek said MedRetreat organized care for 200 people in 2005, about 350 in 2006 and expects to have helped 650 patients this year get treatment in places such as Malaysia and Thailand.
Fresno-based HealthMed Tourism is hoping for similar success.
Owners Emily Higby and Fely Guzman have backgrounds organizing specialty getaway packages -- wine-tasting excursions to South Africa, for example.
Higby became interested in medical tourism because she suffers from polycystic kidney disease, a genetic disorder characterized by the growth of cysts that can reduce kidney function and lead to renal failure.
A kidney transplant could be in her future. "I could probably get it anywhere in Asia for 75 percent less," she said.
Guzman owns a medical staffing company in the Philippines that hires out nurses and physical therapists to Asian health facilities.
The women have toured hospitals in Asia and plan another trip this summer. They said they will send people only to places they have visited personally and where they feel comfortable.
Dodd ran into some difficulty after his operation. He had serious complications after he returned home to Hanford. His stitches opened up, and his local doctor suggested he go back to Mexico to see his surgeon.
He had several additional surgeries there and a "gastric sleeving" to replace the lap-band. He ended up staying in Mexico for about three months.
Today, he talks about his Mexican surgery experience matter-of-factly, boasting of his less-than-200-pound weight on his 5-foot 9-inch frame.
"My quality of life has gone up 100 percent. I'm thinking about cruises," he said, something he would have never considered before.
Dodd said the hospital didn't charge for treating his complications and the additional hospital stay. "Jimmy, you were our guest," he said doctors told him.
He has since retired from his job as a standards inspector at the Kings County Agricultural Commissioner's Office and has canceled his health insurance -- which cost him $500 a month. He said he'll pay cash for routine care and go abroad for surgery.
Dr. Carlos Alessandrini, director and owner of Bajanor Hospital, who came to know Dodd well during his time there, said about 98 percent of the hospital's weight-reduction-surgery patients are from the United States, and the rest mostly from Canada.
He said most of his American patients don't have insurance and pay out of pocket.
The American Hospital Association in Washington doesn't have an official policy on the issue of medical treatment abroad. But spokeswoman Elizabeth Lietz said there are serious considerations people ought to think over before going to foreign hospitals.
"You might not have services and care like you have here," she said.
"The U.S. is recognized globally for its medical treatment, and we are leading the way in advancing treatment of diseases and improving people's health."
Increasing demand for health care abroad prompted the Joint Commission on Accreditation of Healthcare Organizations in 1998 to start an international accreditation branch. A large part of the demand -- at least initially -- came from U.S. companies with American citizens working overseas that wanted to make sure they were offering good care to their employees.
JCAHO International's accreditation has patient care and safety and goals similar to U.S. hospitals.
If more Mexican hospitals sought and received JCAHO accreditation -- the Bajanor Hospital has not -- author Woodman said it might boost credibility, making it even more convenient for Americans in border states to take advantage of lower health-care costs in Mexico.
http://www.sitnews.us/0607news/061907/061907_shns_medtravel.html
Carefull!

Sicko ~ Getting Away With Murder

2007-06-26T00:58:00.000-04:00

Sicko Getting Away With Murder

"They are getting away with murder."
-- Michael Moore (AUDIO VIDEO: Low, High)

Batten the Hatches
Amerigroup Corp.'s chairman and chief executive, Jeff McWaters, says 'SiCKO' is a "headline risk" for the health insurance industry overall

$2,100,000,000,000 Per Year

Sicko now in NYC the film opens June 29th... EVERYWHERE

Contagious'
"...the writer-director's most effective provocation yet."
-- Newsday

"...Moore's most assured, least antagonistic and potentially most important film."
-- New York Daily News

"...sustained standing ovation from the packed audience..."
-- FOX News

Autosomal Recessive PKD

2007-06-23T08:43:00.000-04:00

What is autosomal recessive PKD?
Autosomal recessive PKD is caused by a particular genetic trait that is different from the genetic trait that causes autosomal dominant PKD. Parents who do not have PKD can have a child with the disease if both parents carry the abnormal gene and both pass the gene to their baby. The chance of the child having autosomal recessive PKD when both parents carry the abnormal gene is 25 percent. If only one parent carries the abnormal gene, the baby cannot get autosomal recessive PKD.
The signs of autosomal recessive PKD can begin before birth, so it is often called “infantile PKD.” Children born with autosomal recessive PKD usually develop kidney failure within a few years. Severity of the disease varies. Babies with the worst cases die hours or days after birth. Children with an infantile version may have sufficient renal function for a few years. Some people with autosomal recessive PKD do not develop symptoms until later in childhood and may live into their teens and twenties. People with this juvenile version also usually have liver problems.
What are the symptoms of autosomal recessive PKD?
Children with autosomal recessive PKD experience high blood pressure, urinary tract infections, and frequent urination. The disease usually affects the liver, spleen, and pancreas, resulting in low blood cell counts, varicose veins, and hemorrhoids. Because kidney function is crucial for early physical development, children with autosomal recessive PKD are usually smaller than average size.
How is autosomal recessive PKD diagnosed?
Ultrasound imaging of the fetus or newborn reveals cysts in the kidneys but does not distinguish between the cysts of autosomal recessive and autosomal dominant PKD. Ultrasound examination of kidneys of relatives can be helpful; for example, a parent or grandparent with autosomal dominant PKD cysts could help confirm diagnosis of autosomal dominant PKD in a fetus or child. It is extremely rare, although not impossible, for a person with autosomal recessive PKD to live long enough to become a parent. Because autosomal recessive PKD tends to scar the liver, ultrasound imaging of the liver also aids in diagnosis.
Genetic Diseases
Genes are segments of DNA, the long molecules that reside in each of your body’s cells. The genes, through complex processes, build proteins for growth and maintenance of the body. At conception, DNA—or genes—from both parents are passed to the child.
A genetic disease occurs when one or both parents pass abnormal genes to a child at conception. If receiving an abnormal gene from just one parent is enough to produce a disease in the child, the disease is said to have dominant inheritance. If receiving abnormal genes from both parents is needed to produce disease in the child, the disease is said to be recessive.
The chance of acquiring a dominant disease is higher than the chance of acquiring a recessive disease. A child who receives only one gene copy for a recessive disease at conception will not develop the genetic disease—such as autosomal recessive PKD—but could pass the gene to the following generation.
How is autosomal recessive PKD treated?
Medicines can control high blood pressure in autosomal recessive PKD, and antibiotics can control urinary tract infections. Eating increased amounts of nutritious food improves growth in children with autosomal recessive PKD. In some cases, growth hormones are used. In response to kidney failure, autosomal recessive PKD patients must receive dialysis or transplantation.
http://kidney.niddk.nih.gov/kudiseases/pubs/polycystic/

Sicko available for free

2007-06-18T08:58:00.001-04:00

Michael Moore's latest has been leaked on the web. (via a reader tip)

Update:
Michael Moore is happy about the piracy of his movie and approves the downloads, leading some to believe he did it on purpose

Watch now on goggle video here is the link.
Click here
Approx. 2 hr 3 min.
As a chronically ill person I was shocked , I cried, was outraged, but in the end I was left with a sense of hope.

If you are uninsured, underinsured or fully insured, if you can't afford the meds or treatments suggested by your doctor, it is a must see film! You can't afford not to. Your insurance comapany would rather you did'nt!

Raves a Cannes!
Perhaps a movie that can change our world?
Watch it now, as I am surprised it is still online.

Wishing you good health.

If only ths film had been mainstreamed in time perhaps Edith Isabel Rodriguez would be alive today.

Kidney Notes PKD Blog

2007-06-05T12:03:00.001-04:00

Temsirolimus Is Effective New Treatment For Advanced Renal Cell Carcinoma, Doctors Conclude

GSK's Pazopanib Shows Positive Results In Patients With Advanced Renal Cell Carcinoma, Ovarian Cancer And Soft Tissue Sarcoma

Burch Colposuspension Versus Fascial Sling To Reduce Urinary Stress Incontinence

SICKO Michael Moore's New Movie on U.S. Healthcare System

2007-06-05T12:02:00.000-04:00

June 4th, 2007 12:46 am
Sicko? The truth about the US healthcare system
Michael Moore's new film is a damning indictment of the way the world's richest country looks after those who fall ill. Andrew Gumbel finds out whether his accusations are justified
The Independent
Cynthia Kline knew exactly what was happening to her when she suffered a heart attack at her home in Cambridge, Massachusetts. She took the time to call an ambulance, popped some nitroglycerin tablets she had been prescribed in anticipation of just such an emergency, and waited for help to arrive.
On paper, everything should have gone fine. Unlike tens of millions of Americans, she had health insurance coverage. The ambulance team arrived promptly. The hospital where she had been receiving treatment for her cardiac problems, a private teaching facility affiliated with the Harvard Medical School, was just a few minutes away.
The problem was, the casualty department at the hospital, Mount Auburn, was full to overflowing. And it turned her away. The ambulance took her to another nearby hospital but the treatment she needed, an emergency catheterisation, was not available there. A flurry of phone calls to other medical facilities in the Boston area came up empty. With a few hours, Cynthia Kline was dead.
She died in an American city with one of the highest concentration of top-flight medical specialists in the world. And it happened largely because of America's broken health care system - one where 50 million people are entirely without insurance coverage and tens of millions more struggle to have the treatment they need approved. As a result, medical problems go unattended until they reach crisis point. Patients then rush to hospital casualty departments, where by law they cannot be turned away, overwhelming the system entirely. Everyone - doctors and patients, politicians on both the left and the right - agrees this is an insane way to run a health system.
When Elizabeth Hilsabeck gave birth to premature twins in Austin, Texas, she encountered another kind of insanity. Again, she was insured -- through her husband, who had a good job in banking. But the twins were born when she was barely six months pregnant, and the boy, Parker, developed cerebral palsy. The doctors recommended physical therapy to build up muscle strength and give the boy a fighting chance of learning to walk, but her managed health provider refused to cover it.
The crazy bureaucratic logic was that the policy covered only "rehabilitative" therapy - in other words, teaching a patient a physical skill that has been lost. Since Parker had never walked, the therapy was in essence teaching him a new skill and therefore did not qualify. The Hilsabecks railed, protested, won some small reprieves, but ended up selling their home and moving into a trailer to cover their costs. Elizabeth's husband, Steven, considered taking a new, better-paying job, but chose not to after making careful inquiries about the health insurance coverage. "When is he getting over the cerebral palsy?" a prospective new insurance company representative breezily asked the Hilsabecks. When Elizabeth explained he would never get over it, she was told she was on her own.
Everyone in America has a health-care horror story or knows someone who does. Mostly they are stories of grinding bureaucratic frustration, of phone calls and officials letters and problems with their credit rating, or of people ignoring a slowly deteriorating medical condition because they are afraid that an expensive battery of tests will lead to a course of treatment that could quickly become unaffordable.
Even when things don't go horribly wrong, it is a matter of surviving by the skin of one's teeth.
In Montana, Melissa Anderson can't find affordable insurance because she is self-employed - an increasingly common affliction. When her son Kasey came down with epilepsy two years ago, she was saved only by a recently introduced child health insurance programme specifically tailored to people who aren't poor but can't afford to pay monster medical bills. She herself remains uninsured for anything short of major care needs.
Over the past 15 years, the stories have become less about poor people without the economic means to access the system - although that remains a vast, unsolved problem - and more about the kind of people who have every expectation they will be taken care of. Middle-class people, people with jobs that carry health benefits or - as the problem worsens - people with the sorts of jobs that used to carry robust health benefits which are now more rudimentary and risk their being cut off for a variety of reasons.
This is the morass that Michael Moore has chosen to explore in his latest documentary, Sicko, which goes on release later this month. Moore spends much of the film demonstrating that there is nothing inevitable or necessary about a system that enriches insurance companies and drug manufacturers but shortchanges absolutely everyone else. His searching documentary looks at health care in France, Britain, Canada, and even Cuba - still regarded as a model system for the Third World.
Moore has his share of ghoulishly awful stories. The film kicks off with an uninsured carpenter who has to decide whether to spend $12,000 (£6,000) reattaching his severed ring finger or $60,000 to reattach his severed middle finger. Later on, Moore focuses on a hospital worker whose husband needed a bone marrow transplant to save him from a rare disease. The couple's insurance company refused to cover the transplant because it regarded the treatment as "experimental". The husband died.
Many more stories are collected in a newly published book called Sick: The Untold Story of America's Health Care Crisis, by Jonathan Cohn. A woman in California called Nelene Fox died of breast cancer after she, too, was turned down for a bone marrow transplant by her insurance company. In Georgia, a family whose infant son went into cardiac arrest were forced to take him to a hospital 45 miles away on their insurance carrier's orders. He survived, but suffered permanent disabilities that more prompt treatment might have averted. In New York, an infant called Bryan Jones - whose case was trumpeted all over the local media at the time - died of a heart defect that went undetected because his insurance company kicked him and his mother out of hospital 24 hours after his birth, too soon to carry out the tests that might have spotted the problem.
America's health system offers a tremendous paradox. In medical technology and in the scientific understanding of disease, it is second-to-none. Since doctors are better paid than anywhere else in the world, the country attracts the best of the best. And yet many, if not most, Americans are unable to reap the advantages of this. In fact, as The New York Times columnist Paul Krugman has argued, the very proliferation of research and high-tech equipment is part of the reason for the imbalance in coverage between the privileged few and the increasingly underserved masses. "[The system] compensates for higher spending on insiders, in party, by consigning more people to outsider status --robbing Peter of basic care in order to pay for Paul's state-of-the-art treatment," Krugman wrote recently. "Thus we have the cruel paradox that medical progress is bad for many Americans' health."
Having the system run by for-profit insurance companies turns out to be inefficient and expensive as well as dehumanising. America spends more than twice as much per capita on health care as France, and almost two and a half times as much as Britain. And yet it falls down in almost every key indicator of public health, starting, perhaps, most shockingly, with infant mortality, which is 36 per cent higher than in Britain.
A recent survey by the management consulting company McKinsey estimated the excess bureaucratic costs of managing private insurance policies - scouting for business, processing claims, and hiring "denial management specialists" to tell people why their ailment is not covered by their policy - at about $98bn a year. That, on its own, is significantly more than the $77bn McKinsey calculates it would cost to cover every uninsured American. If the government negotiated bulk purchasing rates for drugs, rather than allowing the pharmaceutical companies to set their own extortionate rates, that would save another $66bn.
Astonishingly, there hasn't been a serious debate about health care in the United States since Bill Clinton, with considerable input from his wife Hillary, tried and failed to overhaul the system in 1994. That, though, may be about to change as the 2008 presidential race heats up. Everyone acknowledges the system is broken. Everyone recognises that 50 million uninsured - including almost 10 million children - is unacceptable in a civilised society.
Even the old, classically American free-market argument - that "socialised" medicine is somehow the first step on a slippery slope towards godless communism - doesn't hold water, because in the absence of a functioning private insurance regime the government ends up picking up about 50 per cent of the overall costs for treatment anyway. The indigent rely on a government programme called Medicaid. The elderly have a government programme called Medicare. And perhaps the most efficient part of the whole system is the Veterans' Administration, a sort of NHS for former servicemen.
Rather like London and Paris in the 19th century, where the authorities belatedly paid attention to outbreaks of cholera once the disease started affecting the rich and middle classes, so the American health crisis may be coming to a head because of the kinds of people who are suffering from its injustices.
Corporate chief executives, for a start, are gagging under the ever-increasing costs of providing coverage to their employees. Starbucks now spends more on health care than it does on coffee beans. Company health costs, as a whole, are at about the same level as corporate profits. In a globalised world where US businesses are competing with low-wage countries such as India and China, that is rapidly becoming unacceptable.
That explains, perhaps, why the chief executive of Wal-Mart, Lee Scott, has made common cause with America's leading service sector union - more commonly a bitter critic of Wal-Mart's labour practices - in calling for a government-run universal health care system by 2012. It's going to be a tough battle. The insurance and pharmaceutical industries bankroll the campaigns of dozens of congressmen and have so far been brutally efficient in protecting their own interests. The Clintons were defeated in 1994 in part because of the power of the industry lobbies. Doing better this time will take singular political courage.
In the meantime, we will hear ever more crazy stories like the one told by Marijon Binder, a former nun in Chicago who ended up being sued by a Catholic hospital for $11,000 because her two-night stay for a heart scare was not considered a worthy charity case. Binder, who works as a live-in companion to a disabled old woman, wrote on all her admission forms that she had no insurance and, in her telling at least, was reassured the hospital would take care of her anyway.
After a year and a monstrous bureaucratic fight that went nowhere, a civil judge promptly absolved her of responsibility for her bill - a lucky outcome, for sure. Binder said: "The whole experience was very demeaning. It made me feel very guilty; it made me feel like a criminal." She is, though, alive and solvent. Not everyone in this system catches the same break.
Michael Moore on Oprah Tuesday
http://www.michaelmoore.com/words/mikeinthenews/index.php?id=9855

Barbaric Holland Lets Future Gameshow Winner Not Die

2007-05-30T09:59:00.000-04:00

Only in Holland can one stand in a windmill next to several policemen dressed as monsters & clowns, and watch a one-legged prostitute in a wooden clog feed her 11-month-old John-baby a de-crusted cocaine sandwich, free of all legal repercussion and woe. Seriously - we actually saw that once.
Well, we didn't see it so much as we drew a picture of it in a grade-school art class. Our teacher changed after that, as did our curriculum. Nonetheless, Holland is a different country. Not only does the Hollish language sound silly & trite, but the whole country likes really strange entertainment too.
In America to entice viewers, television gives out civilised prizes like millions of dollars, love, & several greasy humpings from Flavor Flav. In Holland that's all old hat. That's why their game show prizes are things like - the ability to not die, the power to keep living, & not having to be killed by your poor medical condition because you handled yourself well in the physical challenge.
Basically, there's three contestants with failing kidneys & a terminally ill prize-holder. You can figure it out from there.
Dutch television is such a powerful medium that Eddie Murphy used it to tell the world Mel B might be a skank-ho. The genre also has crazy reality TV - the most recent of which gives the prize of continuing life to the winner. As a brilliant entertainment blog put it like a paragraph ago:
"Basically, there's three contestants with failing kidneys & a terminally ill prize-holder. You can figure it out from there."
Oh - you read that right. Three people (contestants) have failing kidneys, and may just die on a transplant list. A terminally ill show participant will have the power to give life after she dies. As BBC News put it:
"The 37-year-old donor, identified only as Lisa, will make her choice based on the contestants' history, profile and conversation with their family and friends."
The show is called De Grote Donor Show which in Netherlandish for The Big Donor Show. The 'O' in the word 'Show' is shaped like a kidney. De Grote Donor Show is made by the same people who created Big Brother, and premieres on Friday. The whole country's not on the edge of their seat waiting for Friday night. Tons of them hate the idea. One such hater said:
"The set up of the programme bears no relationship to the way decisions are made about transplants in the real world. Living donors can choose altruistically to give one of their kidneys - usually to a family member. If organs become available after someone dies, health professionals with access to detailed information about those waiting for a transplant make objective decisions about who should receive those particular kidneys."
We think the kidneys should just be awarded to the best singer.
That would truly be best for global DNA.

Read More:'Big Brother' Kidney Show Condemned - Sky News

http://www.hecklerspray.com/barbaric-holland-gives-human-kidneys-as-tv-prizes/20068507.php

Kidney Notes PKD Blog

2007-05-30T09:58:00.000-04:00

Angiotech Initiates European Trial Examining The Vascular Wrap(TM) Paclitaxel-eluting Mesh For Dialysis Patients With End-Stage Renal Disease

NY-Presbyterian Hospital/Columbia University Medical Center Doctors Presented At 2007 AUA Meeting

Report On Transurethral Detection And Resection Of Bladder Carcinomas Under White Or 5-ALA Induced Fluroescence Light

How Are We Training The Postgraduate Urologist In Minimally Invasive Surgery?

Challenges For Urologists In Living Kidney Donation

Kidney Notes from PKD Blog

2007-05-29T12:50:00.001-04:00

Mircera Receives Positive Opinion In Europe For The Treatment Of Anaemia Due To Chronic Kidney Disease

Roche Receives Approvable Letter For Mircera In The United States

Roche's New Long-acting ESA* For The Treatment Of Renal Anaemia Receives Positive Opinion In Europe

Three kidney donations make for one close Westport family

2007-05-29T12:49:00.001-04:00

WESTPORT - It's all in the family and this family is very close. Within less than two years, three women in Westport -- including two sisters and a daughter -- will have donated their kidneys to save other family members with polycystic kidney disease.
The two sisters are Christine Earle and Melissa Boudria. Mrs. Earle donated a kidney to her cousin, David McGinn, about a year ago.
On Tuesday, May 8, Mrs. Earle's stepdaughter, Kristin Wilkinson, successfully gave one of her kidneys to David's sister, Charlotte Toddings. In July, Ms. Boudria is scheduled to give a kidney to Charlotte's son, Kevin, who also has Down syndrome.
The family ties may sound complicated but as Ms. Boudria said, "We have an extended family all sorts of ways and we're all extremely close."
Read the rest
http://www.eastbayri.com/story/288999310057821.php

Tolvaptan for chronic heart failure: No antiremodeling benefit observed

2007-05-29T12:48:00.000-04:00

May 29, 2007
Steve Stiles
Washington, DC - A year of treatment with the vasopressin-receptor antagonist tolvaptan (Otsuka America Pharmaceuticals) had no apparent effect on LV end-diastolic volume (LVEDV) in patients with chronic systolic heart failure who were already on evidence-based medical therapy in a small but randomized and placebo-controlled study [1].
However, there was a nonsignificant but "hypothesis-generating" signal of possible long-term benefit in a composite end point that was not prospectively defined—mortality or HF hospitalization—that appears consistent with earlier tolvaptan findings, write the authors, led by Dr James E Udelson (Tufts University School of Medicine, Boston, MA), in their report published online May 18, 2007 in the Journal of the American College of Cardiology.
Tolvaptan is an investigational agent in the US that is also under development for the treatment of hyponatremia and polycystic kidney disease and that has been studied in patients with acute decompensated heart failure (ADHF).
A placebo-controlled international tolvaptan trial that randomized more than 4000 patients with ADHF, called Efficacy of Vasopressin Antagonism in Heart Failure Trial (EVEREST), was published earlier this year [2,3]. As covered by heartwire at the time, those who received the drug in addition to standard IV therapy and who were discharged on it long term showed in-hospital improvements in a composite of patient-assessed clinical status and body weight but no significant clinical advantages out to a year. Its investigators then concluded that tolvaptan could potentially play a role in managing volume overload and alleviating symptoms in patients with ADHF.
In the current study, 240 patients with chronic, NYHA functional class 2-3 heart failure with an LVEF <30%, who were overwhelmingly on diuretics, beta blockers, and either an ACE inhibitor or angiotensin-receptor blocker, were randomized to receive either oral tolvaptan at 30 mg/day or a placebo. Baseline and follow-up quantitative radionuclide ventriculographic studies were available for 91 and 89 patients in the two respective groups.
No significant differences were observed over one year in ventriculographic measures of reverse remodeling, including the primary end point of change in LVEDV and the secondary end points of change in LVEF and in LV end-systolic volume. Nor were there differences throughout the follow-up in vital signs, measures of renal function, levels of the HF prognostic marker brain-type natriuretic peptide, or in self-assessed symptom status or quality of life.
Side effects such as urinary frequency, thirst, and dry mouth were more common in the tolvaptan group, but patients in both groups dropped out of the study due to side effects to the same extent.
In an accompanying editorial, Dr Gian Paolo Rossi (University Hospital, Padova, Italy) writes that the negative study had been designed for tracking any ventricular structural changes but also proposes that a much larger study using higher tolvaptan dosages in a similar population might conceivably show that the drug can improve LV end-diastolic volumes [4].
"All investigators and their institutions received support for this trial from Otsuka America Pharmaceuticals," according to the report, which also states that Udelson and coauthor Dr Marvin A Konstam (Tufts University) are consultants to Otsuka America and that coauthors Drs Christopher Zimmer and Cesare Orlandi are employees of the company.

http://www.theheart.org/article/793479.do

Kidney Notes PKD blog

2007-05-24T06:43:00.001-04:00

Transforming Kidney Transplant Policy

American Association Of Kidney Patients Asks Congressional Leaders To Co-Sponsor Bill

Oxford Transplant Campaign - Seeking A Cure For Kidney And Pancreas Failure, UK

Green Tea May Protect The Bladder From Becoming Inflamed

Five Days Of LEVAQUIN(R) As Effective As 10 Days Of Ciprofloxacin In Complicated Urinary Tract Infections And Acute Pyelonephritis

Quality Versus Quantity: Transforming Kidney Transplant Policy - Alternative Process Proposed By Medical Expert Addresses Challenges

Collaborative Educational Initiative To Focus On Early Treatment Of Chronic Kidney Disease

ACE Inhibitors Help Preserve Kidney Function In IgA Nephropathy

Passing on knowledge about an inherited illness

2007-05-24T06:42:00.000-04:00

5/21/2007 7:35:04 AM
By Jeff Hansel
The Post-Bulletin
Amy Berends of St. Charles doesn't want any more family secrets.
She has come to terms with the knowledge that her grandfather didn't share, before he died, what he knew about his own health. He had polycystic kidney disease, an inherited illness that can have devastating effects for the entire family.
"I remember being so angry. Like, why didn't he just tell us? Why didn't he share that with us," said Berends, who is a registered pediatric nurse.
Polycystic kidney disease causes clusters of cysts to develop in the kidneys, according to MayoClinic.com. Cysts can also form in other organs, and kidney failure can occur.
Families with PKD face many fears, said Mary Welder of Rochester, whose husband Scott's family has been affected. Some people worry if they get diagnosed that they'll lose health insurance, or won't be able to get any. Other's worry employers won't hire them, or they'll lose their jobs. Some fear being treated differently by friends or family, and some simply don't want to face the possibility they might be ill.
But diagnosis and information sharing is important for families, Scott Welder said.
"When somebody has it, there's a strong chance that a portion of the kids can have it too," he said.
There is no cure. "It's kind of one of those things where it's a ticking time bomb," he said.
Berends, who does not have PKD, said her aunt called and described some medical problems.
"I told her, well, that sounds like PKD. But it's inherited," Berends said.
Her aunt thought Berends' grandfather had gotten a letter saying he didn't have the condition. The opposite was true, "but he never told his wife. He didn't tell anybody," Berends said. Many family discussions, sometimes heated ones, ensued as Berends tried to get everyone tested.
"Everybody's a little gun shy. Nobody wants to do it," she said.
A person could live her whole life with PKD and never die from it, Berends said. But it's unpredictable.
"It's a hard thing to have in the family," she said. In her family, she said, "one thing that it did, I think, is pull us closer."
Scott Welder said he has been required to get tested for PKD when he gets life insurance, because his family history of the disease is known.
According to the PKD Foundation, the U.S. House passed a bill to ban discrimination by employers and insurers based on genetics .
http://www.postbulletin.com/newsmanager/templates/localnews_story.asp?z=10&a=294868

PKD Blog Kidney Notes

2007-05-22T11:33:00.000-04:00

Traditional Chinese medicine may help prevent polycystic kidney ...

Passing on knowledge about an inherited illness

Employee gives boss a kidney

iBerkshires Profiles Pittsfield Firefighters Michael Sawicki and ...

IMPACT REPORT: ... or die waiting

Family Ties: Living With Polycystic Kidney Disease

New Agent Found To Fight Genetic Disorders - Zorro-Locked Nucleic Acid

2007-05-07T13:53:00.000-04:00

\A study to appear in the June 2007 issue of The FASEB Journal describes a new agent, called "Zorro-LNA," which has the potential to stop genetic disorders in their tracks. In the study, researchers from the Karolinska Institute in Stockholm, Sweden, describe how they developed Zorro-LNA to bind with both strands of a gene's DNA simultaneously, effectively disabling that gene. This development has clinical implications for virtually every human condition caused by or worsened by dominant defective genes. Examples include: Huntington's disease, familial high cholesterol, polycystic kidney disease, some instances of glaucoma and colorectal cancer, and neurofibromatosis, among others. "Zorro-LNA is a new substance that targets DNA and turns off genes," said co-author Edvard Smith of the Karolinska Institute in Sweden. "It has the potential of becoming a new drug for the treatment of human genetic disease." The findings described in this article significantly raise the possibility that new therapies could arise where defective DNA is deactivated more completely and more thoroughly than ever before. For instance, Zorro-LNA could be used in combination with "RNA interference" (RNAi). Like Zorro-LNA, RNAi has the ability to deactivate genes, but does so by degrading the gene's RNA. In addition, Zorro-LNA could be used to deactivate certain genes in stem cells, which could eventually lead to the development of new cells, tissues, or organs. The discovery of RNAi was recognized by a Nobel Prize award in 2006 to two American scientists. "This is a major development in the treatment not only of genetic diseases, but also of acquired diseases when microbes or toxins cause genes to go awry" said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "One might say these researchers have found a gene-hunter's Holy Grail for which scientists have been hunting for many years. Zorro-LNA should give us a new, safe way of blocking the effects of errors in our genetic repertoire."

### The FASEB Journal is published by the Federation of American Societies for Experimental Biology (FASEB) and is consistently ranked among the top three biology journals worldwide by the Institute for Scientific Information. FASEB comprises 21 nonprofit societies with more than 80,000 members, making it the largest coalition of biomedical research associations in the United States. FASEB advances biological science through collaborative advocacy for research policies that promote scientific progress and education and lead to improvements in human health. Contact: Cody Mooneyhan Federation of American Societies for Experimental Biology

Kidney Notes

2007-05-01T06:04:00.000-04:00

Advagraf® Now Approved Across Europe As A Once-daily Immunosuppressant In Organ Transplantation

In-Depth Research Provides Insight Into Trends, Efficacy And Outcomes Of Cerebral Aneurysm Treatment And The Ongoing Debate: Clip Versus Coil

Intact Specimen Extraction In Laparoscopic Nephrectomy Procedures: Pfannenstiel Versus Expanded Port Site Incisions.

Efficacy Of α-Blockers For The Treatment Of Ureteral Stones

Traditional Chinese medicine may help prevent polycystic kidney disease

2007-05-01T06:03:00.002-04:00

From our ANI CorrespondentWashington, Apr 30: A new study has found that a centuries old Chinese traditional medicine, Triptolide has the potential to stop cyst formation in polycystic kidney disease Triptolide is derived from a Chinese medicinal herb named Lei Gong Teng, which has been used in traditional medicine to treat cancer, inflammation, and auto-immune diseases and, more recently, also has been tested in Phase I clinical trials as an anti-tumour agent.The research holds out hope for what would be the first treatment for the disease other than kidney transplant or frequent dialysis.The study was conducted by a team of researchers led by researcher Dr. Craig Crews at Yale University.During normal kidney development, cells lining the kidney tubules continue growing and dividing until they receive a signal that the tubule is fully formed. The switch that turns on that signal consists of the growth regulatory proteins PKD1 and PKD2, located on hair-like cilia in the lining of the developing tubules. When urine begins flowing through the tubules, the flow bends the cilia that set off the signal that no more growth is needed. In people who have a mutation in one of these growth regulatory proteins, however, the message to stop growing never gets delivered, even when urine is flowing and the cilia are bending. So, never sensing a signal to stop, the cells lining the fully-formed kidney tubules keep right on subdividing and growing. The result of this hyperproliferative, unregulated growth: uncontrolled growth of cells lining the tubules and the formation of large cysts in the kidneys.
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Prize Winners Announced At ISN's World Congress Of Nephrology

2007-05-01T06:03:00.001-04:00

The 2007 Lillian Jean Kaplan International Prize Winners announced at the ISN's World Congress of Nephrology - a celebration of the Foundation's 25 years of "Help and Hope" Vicente Torres and Jing Zhou recognized for advancing critical insight into Polycystic Kidney Disease (PKD) through research of excellence. The International Society of Nephrology (ISN) has announced Vicente Torres, Professor of Medicine and Chair of the Division of Nephrology and Hypertension (Mayo Clinic - USA) and Jing Zhou, Associate Professor of Medicine and Director of the Harvard Center of Polycystic Kidney Disease Research (Harvard University Medical School - USA), as the 2007 winners of the Lillian Jean Kaplan International Prize. Honoring Vicente Torres' seminal contribution at both the clinical and experimental levels of PKD research, his years of dedication to the field have recently culminated in describing the efficacy of vasopressin receptor antagonists in mouse models of PKD. His outstanding efforts serving on the Scientific Advisory Board of the Polycystic Kidney Research Foundation (PKRF) have also been instrumental to advancing the field. Upon receiving the prize Torres expressed his gratitude and sense of optimism toward the future, "It is a great honor to receive this prize. I would like to thank Mr. Thomas Kaplan and the Lillian Jean Kaplan Foundation for this award and the generous support of PKD research as well as both the ISN and the PKD Foundation for sponsoring this event… we are closer than ever today to finding a solution to this disease." Jing Zhou's work, described by Kaplan as 'momentous' has contributed to important breakthroughs within the field such as the first pkd1 knockout mice revealing the roles of the PKD 1 protein, polycystin-1 in embryonic development, as well as the finding that polycystin-2 homologue, polycystin-L, was a calcium-permeable non-selective cation channel. Describing the critical links between calcium, cilia and the cell cycle, Jing Zhou and her group have undoubtedly and fundamentally helped to alter PKD research and attract essential interest from researchers from other related specialties. Commenting on the future directions toward combating the disease Kaplan expressed the ongoing dedication of the Foundation and his positive outlook for research over the coming years, "We are committed to finding ways to spur interest and investment in finding a solution to this disease… I think it is entirely reasonable that in forthcoming years we will see breakthroughs in research and treatment."### 1. Created in 2002, the Lillian Jean Kaplan International Prize for the Advancement in the Understanding of PKD was established through the generosity of Mr. Thomas Kaplan of New York in honor of his mother Lillian Jean Kaplan who died of polycystic kidney disease. The prize was created to recognize those who have increased the understanding and treatment of PKD and to stimulate interest in advancing research that will lead to new treatments and a cure for the disease. 2. The International Society of Nephrology is a not-for-profit society whose mission is the global advancement of nephrology. The Society promotes research and education to prevent and treat kidney disease throughout the world. Further information is available at: http://www.isn-online.org/. Contact: Amanda Wren International Society of Nephrology

Senate gets genetics 'civil rights' bill

2007-05-01T06:02:00.000-04:00

Measure would make denying rights based on predisposition to disease illegal.
By DIANE STAFFORD
The Kansas City Star
It is once again the U.S. Senate’s turn to consider what one bill sponsor calls “landmark civil rights legislation.”
But to pass the Genetic Information Nondiscrimination Act — something the Senate has done twice before — an unnamed senator must be persuaded to release a confidential “hold” placed on the bill, which prevents it from going to the floor.
Supporters view the act as civil rights legislation because it would make it illegal for a health insurer to deny coverage or to charge higher premiums to a healthy person on the basis of a genetic predisposition to a disease.
The act also would bar employers from using genetic information in hiring, promotion or firing decisions.
Lobbying efforts turned to the Senate after the U.S. House on Wednesday passed, 420-3, its version of the act.
That passage came 12 years after it was first introduced in the House.
The Senate had in 2003 and 2005 passed previous versions of the bill unanimously. But it failed to become law because the House did not act.
The White House has issued a statement in support of the legislation, which also would prohibit insurers, employers and labor organizations from demanding genetic testing of individuals or their family members
Organizations such as the PKD Foundation, which advocates for people with polycystic kidney disease, urged the Senate to move forward.
“Regrettably, genetic discrimination in America is alive and well, jeopardizing the insurability and employability for all who inherit disease-causing genes through no fault of their own,” said PKD Foundation President Dan Larson. “While we are thrilled with the U.S. House vote, we now urge the U.S. Senate to move forward and pass this legislation.”
Advances in genetic testing make it possible for people to find out whether they are predisposed to certain diseases. That information, if known, can be used by insurers, who do not want to insure high-risk people, or by employers, who fear high costs, absences or turnover of employees who are genetically disposed to certain diseases or health problems.
Debra Ness, president of the National Partnership for Women and Families, also urged prompt Senate action. Many people who fear discrimination in insurance or employment avoid genetic testing that could help them receive preventive treatments, Ness said.
Source

A Generous Season

2007-04-24T09:37:00.000-04:00

St. Albans, Vermont - April 22, 2007
For a small state, Vermont is big on seasons. Sure, we've got winter, spring, summer, and fall. But we and we alone have ski season, the dreaded mud season, maple sugaring season and walkathon season.
The fundraisers are relatively easy to organize, and relatively successful in separating a donor from his dollar. Dozens of organizations will host walkathons over the next several months. Each does so much good and touches so many lives. One such event Sunday in St. Albans was so personal for Tina Cote and her son Tony Granger. "He takes a lot of medications. His kidneys are down to thirty-three percent function. He needs shots every day. But other than that, he's a normal happy nine year-old," Cote said.
Granger's polycystic kidney disease means he'll need a transplant. It also qualified him for a gift from the Make a Wish Foundation of Vermont. It renovated his bedroom. "I got a flat screen TV, a memory foam bed, an iPod, and some books!" Granger said. When asked what the favorite part of his wish was, Granger answers excitedly, "My TV!"
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