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
Thursday, January 31, 2008
Reproductive issues for adults with autosomal dominant polycystic kidney disease.
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]
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]
Wednesday, January 30, 2008
Scientist triumphs after setback in kidney transplant method
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...
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...
Tuesday, January 29, 2008
Kidney Racket
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 Timesall 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. ...
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 Timesall 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. ...
Monday, January 28, 2008
Northwestern Memorial trial may wean kidney transplant patients off antirejection drugs
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
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
Saturday, January 26, 2008
Kidney Headlines PKD Blog
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
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
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
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
Thursday, January 24, 2008
Breakthrough in Transplants
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
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
Wednesday, January 23, 2008
AAKP 2008 Kidney Beginnings: Live Schedule Announced
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
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
Tuesday, January 22, 2008
Cilia link seeing and peeing
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.
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.
Friday, January 18, 2008
Kidney Headlines PKD Blog
Monday, January 14, 2008
PKD Blog Medical Headlines
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.
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.
Thursday, January 10, 2008
Causes and Risk Factors of Polycystic Kidney Disease
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
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
Wednesday, January 09, 2008
Multiple Renal Cysts, Urinary Concentration Defects, and Pulmonary Emphysematous Changes in Mice Lacking TAZ.
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]
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]
Thursday, January 03, 2008
Pretransplant laparoscopic nephrectomy in adult polycystic kidney disease: a single centre experience.
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]
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]
Tuesday, January 01, 2008
Molecular Basis of Autosomal Recessive Polycystic Kidney Disease (ARPKD).
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]
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]
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