Saturday, December 30, 2006
Polycystic kidney disease: MRI provides an early alert to progression
A new method using magnetic resonance imaging (MRI) accurately tracks structural changes that predict functional changes earlier than standard blood and urine tests in people with autosomal dominant polycystic kidney disease (PKD), according to a study funded by the National Institutes of Health (NIH). PKD is a common inherited condition characterized by cysts that grossly distort the kidneys and liver and by high blood pressure and brain aneurysms (bulges in arteries). Findings are in the May 18 issue of the New England Journal of Medicine.
Researchers found that both small and large cysts and both kidneys grew continuously at steady rates, seemingly tailored to the individual with PKD, regardless of patient age. These structural changes correlate with losses in kidney function, suggesting that MRI can be used to track the major contributor to the progression of PKD, an advance that could speed the discovery of new therapies.
"There is so much variability in the loss of kidney function among PKD patients, even within families with the same altered gene, that it was assumed that cysts and kidneys must grow at variable rates. So it's quite remarkable to find cysts and kidneys in individuals growing at uniform and predictable rates," said Catherine M. Meyers, M.D., a kidney specialist at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). "Our experience is still limited, but this method appears very promising."
Read More:
http://www.doctorslounge.com/nephrology/articles/polycystic_kidney/mri_progression/
Researchers found that both small and large cysts and both kidneys grew continuously at steady rates, seemingly tailored to the individual with PKD, regardless of patient age. These structural changes correlate with losses in kidney function, suggesting that MRI can be used to track the major contributor to the progression of PKD, an advance that could speed the discovery of new therapies.
"There is so much variability in the loss of kidney function among PKD patients, even within families with the same altered gene, that it was assumed that cysts and kidneys must grow at variable rates. So it's quite remarkable to find cysts and kidneys in individuals growing at uniform and predictable rates," said Catherine M. Meyers, M.D., a kidney specialist at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). "Our experience is still limited, but this method appears very promising."
Read More:
http://www.doctorslounge.com/nephrology/articles/polycystic_kidney/mri_progression/
Pax2 gene dosage influences cystogenesis in autosomal dominant polycystic kidney disease.
Stayner C,
Iglesias DM,
Goodyer PR,
Ellis L,
Germino G,
Zhou J,
Eccles MR.
Mutations in PKD1 cause dominant polycystic kidney disease (PKD), characterized by large fluid-filled kidney cysts in adult life, but the molecular mechanism of cystogenesis remains obscure. Ostrom et al. [Dev. Biol., 219, 250-258 (2000)] showed that reduced dosage of Pax2 caused increased apoptosis, and ameliorated cystogenesis in Cpk mutant mice with recessive PKD. Pax2 is expressed in condensing metanephrogenic mesenchyme and arborizing ureteric bud, and plays an important role in kidney development. Transient Pax2 expression during fetal kidney mesenchyme-to-epithelial transition, as well as in nascent tubules, is followed by marked down-regulation of Pax2 expression. Here, we show that in humans with PKD, as well as in Pkd1(del34/del34) mutant mice, Pax2 was expressed in cyst epithelial cells, and facilitated cyst growth in Pkd1(del34/del34) mutant mice. In Pkd1(del34/del34) mutant kidneys, the expression of Pax2 persisted in nascent collecting ducts. In contrast, homozygous Pkd1(del34/del34) fetal mice carrying mutant Pax2 exhibited ameliorated cyst growth, although reduced cystogenesis was not associated with increased apoptosis. Pax2 expression was attenuated in nascent collecting ducts and absent from remnant cysts of Pkd1(del34/del34)/Pax2(1Neu/+) mutant mice. To investigate whether the Pkd1 gene product, Polycystin-1, regulates Pax2, MDCK cells were engineered constitutively expressing wild-type Pkd1; Pax2 protein levels and promoter activity were both repressed in MDCK cells over-expressing Pkd1, but not in cells without transgenic Pkd1. These data suggest that polycystin-1-deficient tubular epithelia persistently express Pax2 in ADPKD, and that Pax2 or its pathway may be an appropriate target for the development of novel therapies for ADPKD.
PMID: 17082250 [PubMed - in process]
Hum Mol Genet. 2006 Dec 15;15(24):3520-8. Epub 2006 Nov
From today's medical headlines:
Study Of Best Treatment Approach For Narrowed Kidney Arteries Joined By MCG
Iglesias DM,
Goodyer PR,
Ellis L,
Germino G,
Zhou J,
Eccles MR.
Mutations in PKD1 cause dominant polycystic kidney disease (PKD), characterized by large fluid-filled kidney cysts in adult life, but the molecular mechanism of cystogenesis remains obscure. Ostrom et al. [Dev. Biol., 219, 250-258 (2000)] showed that reduced dosage of Pax2 caused increased apoptosis, and ameliorated cystogenesis in Cpk mutant mice with recessive PKD. Pax2 is expressed in condensing metanephrogenic mesenchyme and arborizing ureteric bud, and plays an important role in kidney development. Transient Pax2 expression during fetal kidney mesenchyme-to-epithelial transition, as well as in nascent tubules, is followed by marked down-regulation of Pax2 expression. Here, we show that in humans with PKD, as well as in Pkd1(del34/del34) mutant mice, Pax2 was expressed in cyst epithelial cells, and facilitated cyst growth in Pkd1(del34/del34) mutant mice. In Pkd1(del34/del34) mutant kidneys, the expression of Pax2 persisted in nascent collecting ducts. In contrast, homozygous Pkd1(del34/del34) fetal mice carrying mutant Pax2 exhibited ameliorated cyst growth, although reduced cystogenesis was not associated with increased apoptosis. Pax2 expression was attenuated in nascent collecting ducts and absent from remnant cysts of Pkd1(del34/del34)/Pax2(1Neu/+) mutant mice. To investigate whether the Pkd1 gene product, Polycystin-1, regulates Pax2, MDCK cells were engineered constitutively expressing wild-type Pkd1; Pax2 protein levels and promoter activity were both repressed in MDCK cells over-expressing Pkd1, but not in cells without transgenic Pkd1. These data suggest that polycystin-1-deficient tubular epithelia persistently express Pax2 in ADPKD, and that Pax2 or its pathway may be an appropriate target for the development of novel therapies for ADPKD.
PMID: 17082250 [PubMed - in process]
Hum Mol Genet. 2006 Dec 15;15(24):3520-8. Epub 2006 Nov
From today's medical headlines:
Study Of Best Treatment Approach For Narrowed Kidney Arteries Joined By MCG
Thursday, December 28, 2006
Should we pay donors?
From a link on the Corner....Need transplant donors? Pay them
By Virginia Postrel June 10, 2006
When Kaiser Permanente forced kidney patients to transfer from the UC Davis and UC San Francisco transplant centers to its own fledgling program, it shortened their lives -- and created a scandal.But the Kaiser story represents much more than a single health maintenance organization's bad decisions. It reveals a fundamentally broken transplant system, a system that spends its time coping with an ever-growing, life-threatening organ shortage rather than finding ways to reduce or end it.More than 66,000 Americans are languishing on the national waiting list for kidneys -- 10 times the number of kidneys transplanted from deceased donors each year. And the list keeps growing, with a queue of more than 100,000 expected by 2010.Kidney patients literally live or die by where they are on the waiting list. While getting progressively sicker, they must spend several hours at least three times a week hooked up to a dialysis machine, the kidney-disease equivalent of an iron lung (it prolongs your life but imposes a physically debilitating prison sentence).Increasing the supply of deceased donors, while desirable, is difficult -- organ donors have to die healthy and in exactly the right circumstances. But even if every eligible cadaver were harvested, it wouldn't fill the gap. We need more kidney donors, lots more. And they need to be alive.Unfortunately, our laws and culture discourage healthy people from donating organs, as I learned this spring when I gave a kidney to a friend.My parents were appalled. My doctor told me, "You know you can change your mind." Many people couldn't understand why I didn't at least wait until my friend had been on dialysis for a while.This pervasive attitude not only pressures donors to back out, it shapes policies that deter them. Some transplant centers require intrusive, demeaning psychological probes that scare people off. Some bioethicists suspect that donors suffer from a mental disorder, as opposed to being motivated by benevolence or religious conviction.The scrutiny is particularly nasty when healthy people want to give their organs to strangers -- not truly unknown people, mind you, but patients they have gotten to know through Internet sites or press coverage.Many transplant centers flatly refuse "directed donations" to specific strangers. Some argue that it's "unfair" for patients to jump the queue with personal initiative and an appealing story; others insist that such donors aren't to be trusted (they must be either criminal or crazy). Posters at livingdonorsonline.org warn givers to never even mention the Internet, lest their good intentions be thwarted.Sandra Grijalva, a San Francisco woman with polycystic kidney disease, asked Kaiser officials if she could find a donor online -- after having one of her friends disqualified because of high blood pressure. "They said absolutely not," she says. The donor, Kaiser maintained, might someday try to extort money. (So might your cousin, but at least you'd be alive.)Instead of dire possibilities, consider a cold reality: Without tens of thousands of new living donors, most of the people on that very long waiting list are going to suffer and die on dialysis. The transplant community's top priority should be increasing the supply of willing donors.The most obvious way to increase the supply of any scarce commodity -- paying more for it -- is illegal. Federal law blocks transplant centers, patients and insurers from compensating donors in an above-board process, with full legal and medical protections. The growing and inevitable "transplant tourism" industry, and even shadier organ brokers, are the kidney equivalents of back-alley abortionists.Legalized financial incentives would encourage more people to volunteer their organs. Donors would probably still be relatively rare, just as surrogate mothers are. Many, like me, would still help out without payment, just as some people get paid for giving blood or fighting fires while others do it for free.Paying donors need not hurt the poor, any more than paying dialysis centers does. Compensation could, in fact, help low-income Americans, who are disproportionately likely to suffer from kidney disease. A one-year tax holiday for donors would nudge rich people to help. A pool to make up for lost wages (legal, but rare today) would enable many otherwise willing friends and relatives to contribute.But even talking about incentives is taboo to some self-styled patient advocates. On Monday, the American Enterprise Institute will hold a conference in Washington on incentive-based transplant reforms. (It's organized by my kidney recipient, a physician and health-policy scholar at the institute.) When the National Kidney Foundation heard about the conference, its chief executive, John Davis, complained to the institute's president, "We don't see how an AEI forum would contribute substantively to debate on this issue."Davis' group adamantly opposes donor compensation, lobbying against even experimental programs and small tax credits. It's as though the National Parkinson Foundation opposed stem cell research, or thought researchers should work for free.Even a limited market in kidneys would transfer power from the rationing establishment to kidney patients and supportive communities. It would give patients more options. Grijalva, who works with developmentally disabled seniors, would welcome the shift."My biggest fear and my biggest feeling," she says, "is that I'm totally out of control, that these people have the control and they are making all the decisions, and I have absolutely no input whatsoever."Virginia Postrel is a contributing editor to the Atlantic and the author of The Future and Its Enemies and The Substance of Style.
Posted by Emily at 7:44 PM
Labels: transplants- awareness
http://bucketofparts.blogspot.com/2006/12/should-we-pay-donors.html
By Virginia Postrel June 10, 2006
When Kaiser Permanente forced kidney patients to transfer from the UC Davis and UC San Francisco transplant centers to its own fledgling program, it shortened their lives -- and created a scandal.But the Kaiser story represents much more than a single health maintenance organization's bad decisions. It reveals a fundamentally broken transplant system, a system that spends its time coping with an ever-growing, life-threatening organ shortage rather than finding ways to reduce or end it.More than 66,000 Americans are languishing on the national waiting list for kidneys -- 10 times the number of kidneys transplanted from deceased donors each year. And the list keeps growing, with a queue of more than 100,000 expected by 2010.Kidney patients literally live or die by where they are on the waiting list. While getting progressively sicker, they must spend several hours at least three times a week hooked up to a dialysis machine, the kidney-disease equivalent of an iron lung (it prolongs your life but imposes a physically debilitating prison sentence).Increasing the supply of deceased donors, while desirable, is difficult -- organ donors have to die healthy and in exactly the right circumstances. But even if every eligible cadaver were harvested, it wouldn't fill the gap. We need more kidney donors, lots more. And they need to be alive.Unfortunately, our laws and culture discourage healthy people from donating organs, as I learned this spring when I gave a kidney to a friend.My parents were appalled. My doctor told me, "You know you can change your mind." Many people couldn't understand why I didn't at least wait until my friend had been on dialysis for a while.This pervasive attitude not only pressures donors to back out, it shapes policies that deter them. Some transplant centers require intrusive, demeaning psychological probes that scare people off. Some bioethicists suspect that donors suffer from a mental disorder, as opposed to being motivated by benevolence or religious conviction.The scrutiny is particularly nasty when healthy people want to give their organs to strangers -- not truly unknown people, mind you, but patients they have gotten to know through Internet sites or press coverage.Many transplant centers flatly refuse "directed donations" to specific strangers. Some argue that it's "unfair" for patients to jump the queue with personal initiative and an appealing story; others insist that such donors aren't to be trusted (they must be either criminal or crazy). Posters at livingdonorsonline.org warn givers to never even mention the Internet, lest their good intentions be thwarted.Sandra Grijalva, a San Francisco woman with polycystic kidney disease, asked Kaiser officials if she could find a donor online -- after having one of her friends disqualified because of high blood pressure. "They said absolutely not," she says. The donor, Kaiser maintained, might someday try to extort money. (So might your cousin, but at least you'd be alive.)Instead of dire possibilities, consider a cold reality: Without tens of thousands of new living donors, most of the people on that very long waiting list are going to suffer and die on dialysis. The transplant community's top priority should be increasing the supply of willing donors.The most obvious way to increase the supply of any scarce commodity -- paying more for it -- is illegal. Federal law blocks transplant centers, patients and insurers from compensating donors in an above-board process, with full legal and medical protections. The growing and inevitable "transplant tourism" industry, and even shadier organ brokers, are the kidney equivalents of back-alley abortionists.Legalized financial incentives would encourage more people to volunteer their organs. Donors would probably still be relatively rare, just as surrogate mothers are. Many, like me, would still help out without payment, just as some people get paid for giving blood or fighting fires while others do it for free.Paying donors need not hurt the poor, any more than paying dialysis centers does. Compensation could, in fact, help low-income Americans, who are disproportionately likely to suffer from kidney disease. A one-year tax holiday for donors would nudge rich people to help. A pool to make up for lost wages (legal, but rare today) would enable many otherwise willing friends and relatives to contribute.But even talking about incentives is taboo to some self-styled patient advocates. On Monday, the American Enterprise Institute will hold a conference in Washington on incentive-based transplant reforms. (It's organized by my kidney recipient, a physician and health-policy scholar at the institute.) When the National Kidney Foundation heard about the conference, its chief executive, John Davis, complained to the institute's president, "We don't see how an AEI forum would contribute substantively to debate on this issue."Davis' group adamantly opposes donor compensation, lobbying against even experimental programs and small tax credits. It's as though the National Parkinson Foundation opposed stem cell research, or thought researchers should work for free.Even a limited market in kidneys would transfer power from the rationing establishment to kidney patients and supportive communities. It would give patients more options. Grijalva, who works with developmentally disabled seniors, would welcome the shift."My biggest fear and my biggest feeling," she says, "is that I'm totally out of control, that these people have the control and they are making all the decisions, and I have absolutely no input whatsoever."Virginia Postrel is a contributing editor to the Atlantic and the author of The Future and Its Enemies and The Substance of Style.
Posted by Emily at 7:44 PM
Labels: transplants- awareness
http://bucketofparts.blogspot.com/2006/12/should-we-pay-donors.html
Wednesday, December 27, 2006
PKD News
Protein Essential For Kidney-to-Bladder Urine Transfer
Polyomavirus (BK) in Pediatric Renal Transplants: Evaluation of Viremic Patients With and without BK Associated NephritisTuesday, 26 December 2006BERKELEY, CA (UroToday.com) - Polyoma BK virus recently emerged as a significant cause of complication in renal transplantations, which typically may lead to renal dysfunction and overall graft loss secondary to nephritis caused by the BK virus. Hymes, et al reported on their management and outcome of 20 children who developed BK viremia.read more
Efficacy of Tricyclic Antidepressant is Associated with Beta2-Adrenoceptor Genotype in Patients with Interstitial CystitisWednesday, 27 December 2006BERKELEY, CA (UroToday.com) - Tricyclic antidepressant therapy (amitriptyline in particular) is effective in treating the symptoms of PBS/IC. These drugs block the active transport system that is involved in the re-uptake of serotonin and noradrenaline.read more
Pair who bought kidney get suspended termsThe Japan Times, Japan - 21 hours ago... branch of the Matsuyama District Court sentenced a company executive and his wife Tuesday to suspended one-year prison terms for buying a kidney he needed for ...
Polyomavirus (BK) in Pediatric Renal Transplants: Evaluation of Viremic Patients With and without BK Associated NephritisTuesday, 26 December 2006BERKELEY, CA (UroToday.com) - Polyoma BK virus recently emerged as a significant cause of complication in renal transplantations, which typically may lead to renal dysfunction and overall graft loss secondary to nephritis caused by the BK virus. Hymes, et al reported on their management and outcome of 20 children who developed BK viremia.read more
Efficacy of Tricyclic Antidepressant is Associated with Beta2-Adrenoceptor Genotype in Patients with Interstitial CystitisWednesday, 27 December 2006BERKELEY, CA (UroToday.com) - Tricyclic antidepressant therapy (amitriptyline in particular) is effective in treating the symptoms of PBS/IC. These drugs block the active transport system that is involved in the re-uptake of serotonin and noradrenaline.read more
Pair who bought kidney get suspended termsThe Japan Times, Japan - 21 hours ago... branch of the Matsuyama District Court sentenced a company executive and his wife Tuesday to suspended one-year prison terms for buying a kidney he needed for ...
Tuesday, December 26, 2006
Warning Signs of Kidney and Urinary Tract Diseases
High blood pressure
Protein and/or blood in the urine
Creatinine and BUN blood tests outside the normal range*
Glomerular filtration rate (GFR) of less than 90**
More frequent urination, particularly at night; difficult or painful urination
Puffiness around eyes, swelling of hands and feet
* BUN and creatinine are wastes that build up in the blood when your kidney function is reduced.
** GFR (a measure of kidney function) is estimated from a blood creatinine test. In some people, a GFR of 60 to 89 may be normal.
Updated: 05/14/04
See also in this A-Z guide:
Interstitial Cystitis
Urinary Tract Infections
All health information in this A-Z Guide has been approved for medical accuracy by the Scientific Advisory Board of the National Kidney Foundation. This information was current as of the date listed at the top of the page. Our Scientific Advisory Board members.
If you would like to become a volunteer and find out more about what's happening where you live, contact your local NKF Affiliate.
Protein and/or blood in the urine
Creatinine and BUN blood tests outside the normal range*
Glomerular filtration rate (GFR) of less than 90**
More frequent urination, particularly at night; difficult or painful urination
Puffiness around eyes, swelling of hands and feet
* BUN and creatinine are wastes that build up in the blood when your kidney function is reduced.
** GFR (a measure of kidney function) is estimated from a blood creatinine test. In some people, a GFR of 60 to 89 may be normal.
Updated: 05/14/04
See also in this A-Z guide:
Interstitial Cystitis
Urinary Tract Infections
All health information in this A-Z Guide has been approved for medical accuracy by the Scientific Advisory Board of the National Kidney Foundation. This information was current as of the date listed at the top of the page. Our Scientific Advisory Board members.
If you would like to become a volunteer and find out more about what's happening where you live, contact your local NKF Affiliate.
PKD Blog News
Kidney Stones Occurring More Often In Children
Therapy Modulates Highly Sensitized Immune System To Let Mother Give Kidney To Daughter
Medical Society Advises Physicians On How To Minimize Dangers Of Contrast Dye - To Prevent Kidney Damage After Imaging Procedures
Link Between Nanoparticles And Kidney Stones
Kidney Cancer Panel
Bald, Happy And Vulnerable: Bacteria AfterTreatments For Urinary Infections
Therapy Modulates Highly Sensitized Immune System To Let Mother Give Kidney To Daughter
Medical Society Advises Physicians On How To Minimize Dangers Of Contrast Dye - To Prevent Kidney Damage After Imaging Procedures
Link Between Nanoparticles And Kidney Stones
Kidney Cancer Panel
Bald, Happy And Vulnerable: Bacteria AfterTreatments For Urinary Infections
Wednesday, December 20, 2006
Happy Holidays!
Happy ( insert celebration Here)
form all our bloggers!
Wishing all a renewed sence of hope and faith for the new year
Tuesday, December 19, 2006
Recent PKD Related Headlines
Friday, December 15, 2006
Fiscal Year 2007 Budget Request
DEPARTMENT OF HEALTH AND HUMAN SERVICESNATIONAL INSTITUTES OF HEALTHFiscal Year 2007 Budget RequestWitness appearing before theHouse Subcommittee on Labor-HHS-Education AppropriationsGriffin P. Rodgers, M.D., M.A.C.P., Acting DirectorNational Institute of Diabetes and Digestive and Kidney Diseases.
Excerpt:
Chronic diseases pose some of the greatest health challenges to the Nation today. These diseases and their symptoms range in severity, but are often debilitating and sometimes fatal. Some impair fundamental body processes, such as metabolism, while others target the kidneys, liver, and other vital organs and systems. Though their causes and ultimate effects on health may differ, chronic diseases share the grim features of constant affliction and impaired quality-of-life. The burden of chronic diseases within NIDDK's research purview is immense. Recent estimates using national health survey data reveal that diabetes (type 1 and type 2) affects nearly 21 million Americans. About 20 million Americans have chronically impaired kidney function, which places them at increased risk for irreversible kidney failure (end stage renal disease) and death. Digestive diseases, such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and liver and biliary diseases, wreak havoc with people's lives. "Benign" diseases of the bladder and lower urinary tract, including urinary incontinence and prostate diseases, can be devastating. These chronic diseases also exact a heavy economic toll. For example, the healthcare and indirect costs of diabetes and its complications totaled $132 billion in 2002. The painful, debilitating symptoms of IBS and the bladder disease interstitial cystitis (IC) result in loss of work and increased medical costs. Costs of chronic diseases that strike the digestive system, kidneys, and bladder run into the tens of billions of dollars.
The tremendous human and monetary costs of chronic disease are matched only by the extraordinary interventions often needed just to preserve life. Organ transplantation and kidney dialysis are but two examples. Although these are extreme measures for the sickest patients, they represent some of the victories achieved by biomedical research in reducing morbidity and mortality from advanced chronic disease. Our goal is to improve these treatments, while we simultaneously seek prevention strategies. For example, whole liver transplantation from deceased donors is a successful treatment for liver failure, but is limited by a shortage of donor organs. A new NIDDK clinical network (A2ALL) is maximizing this treatment option in adults by assessing the safety and outcomes, for both patients and donors, of new procedures that use partial liver transplants from living donors--thereby increasing the potential donor pool. Similarly, we are addressing the diminished quality-of-life and low five-year survival rates under current dialysis treatment, which is typically administered three times weekly. A new clinical trial will evaluate the effectiveness of daily dialysis.
http://www.niddk.nih.gov/federal/planning/FY2007-Budget-Testimony.htm
Excerpt:
Chronic diseases pose some of the greatest health challenges to the Nation today. These diseases and their symptoms range in severity, but are often debilitating and sometimes fatal. Some impair fundamental body processes, such as metabolism, while others target the kidneys, liver, and other vital organs and systems. Though their causes and ultimate effects on health may differ, chronic diseases share the grim features of constant affliction and impaired quality-of-life. The burden of chronic diseases within NIDDK's research purview is immense. Recent estimates using national health survey data reveal that diabetes (type 1 and type 2) affects nearly 21 million Americans. About 20 million Americans have chronically impaired kidney function, which places them at increased risk for irreversible kidney failure (end stage renal disease) and death. Digestive diseases, such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and liver and biliary diseases, wreak havoc with people's lives. "Benign" diseases of the bladder and lower urinary tract, including urinary incontinence and prostate diseases, can be devastating. These chronic diseases also exact a heavy economic toll. For example, the healthcare and indirect costs of diabetes and its complications totaled $132 billion in 2002. The painful, debilitating symptoms of IBS and the bladder disease interstitial cystitis (IC) result in loss of work and increased medical costs. Costs of chronic diseases that strike the digestive system, kidneys, and bladder run into the tens of billions of dollars.
The tremendous human and monetary costs of chronic disease are matched only by the extraordinary interventions often needed just to preserve life. Organ transplantation and kidney dialysis are but two examples. Although these are extreme measures for the sickest patients, they represent some of the victories achieved by biomedical research in reducing morbidity and mortality from advanced chronic disease. Our goal is to improve these treatments, while we simultaneously seek prevention strategies. For example, whole liver transplantation from deceased donors is a successful treatment for liver failure, but is limited by a shortage of donor organs. A new NIDDK clinical network (A2ALL) is maximizing this treatment option in adults by assessing the safety and outcomes, for both patients and donors, of new procedures that use partial liver transplants from living donors--thereby increasing the potential donor pool. Similarly, we are addressing the diminished quality-of-life and low five-year survival rates under current dialysis treatment, which is typically administered three times weekly. A new clinical trial will evaluate the effectiveness of daily dialysis.
http://www.niddk.nih.gov/federal/planning/FY2007-Budget-Testimony.htm
Insuficiencia renal: Coma bien para sentirse bien durante su tratamiento de hemodiálisis
En está página:
Información acerca del uso de este folleto
¿Cómo afectan los alimentos a mi tratamiento de hemodiálisis?
¿Qué necesito saber acerca de los líquidos?
¿Qué necesito saber acerca del potasio?
¿Qué necesito saber acerca del fósforo?
¿Qué necesito saber acerca de las proteínas?
¿Qué necesito saber acerca del sodio?
¿Qué necesito saber acerca de las calorías?
¿Debo tomar vitaminas y minerales?
Fuentes informativas
Agradecimientos
Información acerca del uso de este folleto
Cuando usted inicia el tratamiento de hemodiálisis, usted debe realizar muchos cambios en su vida. Estar consciente de los alimentos que come le brindará una mejor salud. Este librito le ayudará a escoger los alimentos correctos.
Utilice este folleto con el asesoramiento de un nutricionista para aprender a comer bien para sentirse bien durante su tratamiento de hemodiálisis. Lea una sección a la vez. Luego haga los ejercicios con su nutricionista.
Una vez que haya terminado todos los ejercicios, guarde este librito para acordarse de los alimentos que puede comer y de los alimentos que debe evitar.
¿Cómo afectan los alimentos a mi tratamiento de hemodiálisis?
Los alimentos le dan energía y ayudan a que su cuerpo se repare a sí mismo. Los alimentos se digieren en su estómago e intestinos. Su sangre recoge nutrientes de los alimentos digeridos y los transporta a todas las células de su cuerpo. Estas células absorben los nutrientes de su sangre y depositan los productos de desecho en el torrente sanguíneo. Cuando sus riñones estaban sanos, éstos trabajaban las 24 horas del día para eliminar los productos de desecho de su sangre. Los productos de desecho eran eliminados de su cuerpo por medio de su orina. Otros productos de degradación son eliminados al defecar.
http://kidney.niddk.nih.gov/spanish/pubs/eatright/
Información acerca del uso de este folleto
¿Cómo afectan los alimentos a mi tratamiento de hemodiálisis?
¿Qué necesito saber acerca de los líquidos?
¿Qué necesito saber acerca del potasio?
¿Qué necesito saber acerca del fósforo?
¿Qué necesito saber acerca de las proteínas?
¿Qué necesito saber acerca del sodio?
¿Qué necesito saber acerca de las calorías?
¿Debo tomar vitaminas y minerales?
Fuentes informativas
Agradecimientos
Información acerca del uso de este folleto
Cuando usted inicia el tratamiento de hemodiálisis, usted debe realizar muchos cambios en su vida. Estar consciente de los alimentos que come le brindará una mejor salud. Este librito le ayudará a escoger los alimentos correctos.
Utilice este folleto con el asesoramiento de un nutricionista para aprender a comer bien para sentirse bien durante su tratamiento de hemodiálisis. Lea una sección a la vez. Luego haga los ejercicios con su nutricionista.
Una vez que haya terminado todos los ejercicios, guarde este librito para acordarse de los alimentos que puede comer y de los alimentos que debe evitar.
¿Cómo afectan los alimentos a mi tratamiento de hemodiálisis?
Los alimentos le dan energía y ayudan a que su cuerpo se repare a sí mismo. Los alimentos se digieren en su estómago e intestinos. Su sangre recoge nutrientes de los alimentos digeridos y los transporta a todas las células de su cuerpo. Estas células absorben los nutrientes de su sangre y depositan los productos de desecho en el torrente sanguíneo. Cuando sus riñones estaban sanos, éstos trabajaban las 24 horas del día para eliminar los productos de desecho de su sangre. Los productos de desecho eran eliminados de su cuerpo por medio de su orina. Otros productos de degradación son eliminados al defecar.
http://kidney.niddk.nih.gov/spanish/pubs/eatright/
PKD Blog Medical Headlines
Steroid-free Medication Lowers Rejection Rate For Kidney Transplants - Alternate Treatments Avoid The Side Effects Of Long-Term Steroid Use
Salvage Extravesical Ureteral Reimplantation After Failed Endoscopic Surgery For Vesicoureteral Reflux
Preventing Retrograde Stone Displacement During Pneumatic Lithotripsy For Ureteral Calculi Using Lidocaine Jelly
The Effects Of Palifermin In Patients With Impaired Kidney Function: Study In The Journal Of Clinical Pharmacology
Thirty-fifth Patient Enrolled In The NeuroVasx CPAX Aneurysm Treatment System Clinical Study
Salvage Extravesical Ureteral Reimplantation After Failed Endoscopic Surgery For Vesicoureteral Reflux
Preventing Retrograde Stone Displacement During Pneumatic Lithotripsy For Ureteral Calculi Using Lidocaine Jelly
The Effects Of Palifermin In Patients With Impaired Kidney Function: Study In The Journal Of Clinical Pharmacology
Thirty-fifth Patient Enrolled In The NeuroVasx CPAX Aneurysm Treatment System Clinical Study
Friday, December 08, 2006
Use of Subcutaneous Injections of Epogen for Dialysis Patients Could Save Medicare $537M Annually
Administering the anti-anemia drug Epogen to kidney dialysis patients by subcutaneous injections rather than intravenously could save the federal government hundreds of millions of dollars annually, the Boston Globe reports. Epogen, which is manufactured by California-based Amgen, is administered to kidney disease patients on dialysis to replenish red blood cells. About 95% of the 325,000 U.S. residents on dialysis receive Epogen intravenously, although studies have found that about 30% less Epogen is required if the drug is injected under the skin, the Globe reports. Medicare spends close to $2 billion per year on Epogen, more than on any other drug. According to a study conducted by researchers at Detroit-based Henry Ford Hospital and published in the American Journal of Kidney Disease, administering Epogen subcutaneously rather than intravenously would save the federal government as much as $537 million annually. The study found that the annual Epogen cost per dialysis patient in 2002 was $6,000. Researchers determined that switching to subcutaneous injections would save up to 30%, or $1,761, per patient. A separate study of dialysis clinics in 2004 found that patients received 21% less Epogen when given subcutaneous injections, the Globe reports. Last year, FDA allowed Amgen to change the label on Epogen to state that intravenous delivery is preferred because of a rare disorder called pure red cell aplasia that developed in 175 patients from 1998 through 2003. Those patients received Eprex, a drug similar to Epogen that is manufactured by a Johnson & Johnson subsidiary. J&J said the cases likely were linked to rubber stoppers in some of its syringes and that the outbreak ended after the stoppers were replaced.
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Radiant Medical Trial Shows Promising Results In Preventing Kidney Damage
Endovascular therapeutic hypothermia may help prevent radiocontrast nephropathy (RCN), a cause of kidney failure, according to the results of a clinical feasibility trial presented at the recent American Heart Association's Scientific Sessions 2006 in Chicago
Radiant Medical, Inc., a private medical technology company developing endovascular temperature therapy products, sponsored the COOL RCN (COOLing to Prevent RadioContrast Nephropathy in Patients Undergoing Diagnostic or Interventional Catheterization) Pilot Trial, a feasibility study conducted at eight international medical centers. The study was designed to evaluate the feasibility of preventing RCN, an acute decline in kidney function after the administration of contrast agents, in high-risk patients. Patients were treated with the new Radiant Medical endovascular temperature therapy system, a venous heat exchange catheter that enables very rapid induction of mild hypothermia and rewarming.
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Radiant Medical, Inc., a private medical technology company developing endovascular temperature therapy products, sponsored the COOL RCN (COOLing to Prevent RadioContrast Nephropathy in Patients Undergoing Diagnostic or Interventional Catheterization) Pilot Trial, a feasibility study conducted at eight international medical centers. The study was designed to evaluate the feasibility of preventing RCN, an acute decline in kidney function after the administration of contrast agents, in high-risk patients. Patients were treated with the new Radiant Medical endovascular temperature therapy system, a venous heat exchange catheter that enables very rapid induction of mild hypothermia and rewarming.
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Thursday, December 07, 2006
Patriots tight end Daniel Graham was ready to give up his career.
By HOWARD ULMAN
THE ASSOCIATED PRESS
FOXBORO - Patriots tight end Daniel Graham was ready to give up his career.
His big brother needed a kidney and Graham, one of the NFL's best blocking tight ends, puts family ahead of football. He was willing to donate one of his.
''I've got a bigger role in life,'' he said. ''This is my brother we're talking about. It's a matter of life and death. I can give up what I do for a living. I can find something else to do. If it came down to it, I was ready to do it.''
The surgery took place Tuesday in St. Louis. Jason Graham, 33, got a kidney from his mother Marilyn, who was a better match. Daniel, 28, was there for the operation and returned from the hospital Tuesday night in time to practice with his teammates, as usual, yesterday.
Both his mother and brother are doing fine, he said.
Tomorrow will be another unusual and happy day for Graham. That's when he'll attend his first Patriots captains meeting. Coach Bill Belichick added him to that group after practice last Friday, a rarity during the season.
''Coach came up speaking. First he asked how my family was doing, then he brought the information to me,'' Graham said. ''He told me the captains and the coaches liked my work ethic, the physical game I play and everything.''
He was surprised because the move came during the season. The only other time Belichick added a captain after the season began was in 2003 when he did it with safety Rodney Harrison. The other captains are Tom Brady, Troy Brown, Richard Seymour, Tedy Bruschi, Mike Vrabel and Larry Izzo.
''It's really not a goal of mine,'' said Graham, who was a captain at Thomas Jefferson High in Denver. ''I hope a lot of younger guys look up to how I play and what I do off the field. But when coach came up to me and added me onto the captains group, it was an honor for me. I told him that.''
The soft-spoken Graham has been a solid contributor since the Patriots drafted him in the first round out of Colorado in 2002. He started six of the 12 games he played as a rookie. In his first four seasons he had 99 catches, fewer than 25 per year.
And this year he has only 13 catches in eight games while another tight end, third-year pro Benjamin Watson, has emerged as the team's leading receiver with 48 catches for a team-high 638 yards going into Sunday's game at Miami.
But few tight ends block as well the 257-pound Graham.
''There's a toughness. There's teamwork,'' Brady said. ''Dan is a guy who does what the coach asks him. 'Dan, you're going to come in and run block.' No problem. 'Dan, you're going to come in and run a seam route and make a diving catch.' No problem.''
That's the kind of player Belichick seeks in a captain. The other seven who fill those roles fit that description.
During their five seasons together, Brady has come to depend on Graham to run precise patterns, catch passes and keep 300-pound defensive linemen from sacking him.
''I've been through a lot with Dan,'' Brady said. ''He's one of the core guys we have.''
DOLPHINS' BROWN OUT FOR GAME AGAINST PATS: Leading rusher Ronnie Brown will miss his second game in a row Sunday against New England because of a broken left hand. His hand was fitted with a new cast this week for the injury suffered at Detroit on Nov. 23.
''It's difficult being able to protect the injury because of the positon he plays,'' coach Nick Saban said. ''We have to wait until he mends to protect him well enough that he wouldn't be at risk of reinjury.''
Sammy Morris will make his second start of the season in place of Brown, who said he might be able to play at Buffalo on Dec. 17.
(Published: December 7, 2006)
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THE ASSOCIATED PRESS
FOXBORO - Patriots tight end Daniel Graham was ready to give up his career.
His big brother needed a kidney and Graham, one of the NFL's best blocking tight ends, puts family ahead of football. He was willing to donate one of his.
''I've got a bigger role in life,'' he said. ''This is my brother we're talking about. It's a matter of life and death. I can give up what I do for a living. I can find something else to do. If it came down to it, I was ready to do it.''
The surgery took place Tuesday in St. Louis. Jason Graham, 33, got a kidney from his mother Marilyn, who was a better match. Daniel, 28, was there for the operation and returned from the hospital Tuesday night in time to practice with his teammates, as usual, yesterday.
Both his mother and brother are doing fine, he said.
Tomorrow will be another unusual and happy day for Graham. That's when he'll attend his first Patriots captains meeting. Coach Bill Belichick added him to that group after practice last Friday, a rarity during the season.
''Coach came up speaking. First he asked how my family was doing, then he brought the information to me,'' Graham said. ''He told me the captains and the coaches liked my work ethic, the physical game I play and everything.''
He was surprised because the move came during the season. The only other time Belichick added a captain after the season began was in 2003 when he did it with safety Rodney Harrison. The other captains are Tom Brady, Troy Brown, Richard Seymour, Tedy Bruschi, Mike Vrabel and Larry Izzo.
''It's really not a goal of mine,'' said Graham, who was a captain at Thomas Jefferson High in Denver. ''I hope a lot of younger guys look up to how I play and what I do off the field. But when coach came up to me and added me onto the captains group, it was an honor for me. I told him that.''
The soft-spoken Graham has been a solid contributor since the Patriots drafted him in the first round out of Colorado in 2002. He started six of the 12 games he played as a rookie. In his first four seasons he had 99 catches, fewer than 25 per year.
And this year he has only 13 catches in eight games while another tight end, third-year pro Benjamin Watson, has emerged as the team's leading receiver with 48 catches for a team-high 638 yards going into Sunday's game at Miami.
But few tight ends block as well the 257-pound Graham.
''There's a toughness. There's teamwork,'' Brady said. ''Dan is a guy who does what the coach asks him. 'Dan, you're going to come in and run block.' No problem. 'Dan, you're going to come in and run a seam route and make a diving catch.' No problem.''
That's the kind of player Belichick seeks in a captain. The other seven who fill those roles fit that description.
During their five seasons together, Brady has come to depend on Graham to run precise patterns, catch passes and keep 300-pound defensive linemen from sacking him.
''I've been through a lot with Dan,'' Brady said. ''He's one of the core guys we have.''
DOLPHINS' BROWN OUT FOR GAME AGAINST PATS: Leading rusher Ronnie Brown will miss his second game in a row Sunday against New England because of a broken left hand. His hand was fitted with a new cast this week for the injury suffered at Detroit on Nov. 23.
''It's difficult being able to protect the injury because of the positon he plays,'' coach Nick Saban said. ''We have to wait until he mends to protect him well enough that he wouldn't be at risk of reinjury.''
Sammy Morris will make his second start of the season in place of Brown, who said he might be able to play at Buffalo on Dec. 17.
(Published: December 7, 2006)
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Retroperitoneoscopic Managementof Infected Cysts in Adult Polycystic Kidney Disease
K. Hemala, N.P. Guptaa, T.P. Rajeeva, Monish Arona, Dipankar Bhowmikb, Rajeev JaincDepartments ofaUrology,bNephrology andcRadiodiagnosis, All-India Institute of Medical Sciences, New Delhi, India
Address of Corresponding Author
Urologia Internationalis 1999;62:40-43 (DOI: 10.1159/000030354)
Key Words
Laparoscopy
Retroperitoneoscopy
Adult polycystic kidney
Cyst infection
Abstract
Conservative measures are the mainstay of therapy in adult polycystic kidney disease (APKD). Pain, infection and obstructive uropathy are the major indications for intervention. Chronic pain has been treated with narcotic analgesics, needle aspiration of dominant cysts, and open renal cyst decortication. Laparoscopic cyst decortication, by either transperitoneal or retroperitoneal access, is a new emerging option with similar efficacy to open surgery and less morbidity. Cyst infection in these patients responds poorly to commonly used antibiotics. Patients with refractory cyst infection may even require nephrectomy. Herein, we present 2 cases with APKD that were treated by retroperitoneoscopic decortication for painful and infected cysts. Both patients showed prompt and sustained improvement in symptoms, with minimal morbidity and short convalescence. This approach has not hitherto been described for infected cysts in APKD. The retroperitoneoscopic route should be preferred in the presence of infected cysts so as to prevent intraperitoneal contamination.
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Address of Corresponding Author
Urologia Internationalis 1999;62:40-43 (DOI: 10.1159/000030354)
Key Words
Laparoscopy
Retroperitoneoscopy
Adult polycystic kidney
Cyst infection
Abstract
Conservative measures are the mainstay of therapy in adult polycystic kidney disease (APKD). Pain, infection and obstructive uropathy are the major indications for intervention. Chronic pain has been treated with narcotic analgesics, needle aspiration of dominant cysts, and open renal cyst decortication. Laparoscopic cyst decortication, by either transperitoneal or retroperitoneal access, is a new emerging option with similar efficacy to open surgery and less morbidity. Cyst infection in these patients responds poorly to commonly used antibiotics. Patients with refractory cyst infection may even require nephrectomy. Herein, we present 2 cases with APKD that were treated by retroperitoneoscopic decortication for painful and infected cysts. Both patients showed prompt and sustained improvement in symptoms, with minimal morbidity and short convalescence. This approach has not hitherto been described for infected cysts in APKD. The retroperitoneoscopic route should be preferred in the presence of infected cysts so as to prevent intraperitoneal contamination.
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Enjoy Your Own Recipes Using Less Protein:
A guide for people with chronic kidney disease
If you have just learned that you have chronic kidney disease (CKD), your doctor may tell you to start limiting the protein in your diet. Changing your diet to meet your body's lower protein needs and still using the foods and recipes you are used to can be difficult. This fact sheet has ideas and tips to help you lower the protein in your favorite recipes, using the foods you normally use every day.
Why do I need to eat less protein?Protein is needed for growth, upkeep and repair of all parts of your body. Protein is found in almost all foods. When your body breaks down and uses the food you eat, a waste product called urea is made. When your kidneys are not working well, urea is not removed as it should be. Urea then builds up inside your body. Side effects of a high urea level are fatigue (tiredness) and poor appetite. By decreasing the amount of protein you eat, you can help your kidneys have a lighter work load, with less urea to clean out.
What foods have the most protein?There are two types of protein in the food we eat:
Animal protein is called high-value protein. It is easier for your body to use. Examples of high-value animal proteins are: red meat, chicken, turkey, pork, eggs and dairy products.* It is very important for you to eat enough high-value protein to keep your body healthy.* Dairy products are high-value protein, but are also high in phosphorus. You may need to use less dairy products in your diet to control your blood level of phosphorus.
Vegetable or plant proteins are low-value proteins. Examples of low-value proteins are: bread, cereals, dried beans, nuts, rice, pasta or noodles and vegetables.
A dietitian trained to work with those who have CKD can help you balance your protein.
How can I eat less protein and still feel like I am eating enough?Here are some tips to help you stretch protein foods so that a smaller amount will still feel like enough.
Sandwiches
Fill up sandwiches with lettuce, alfalfa sprouts, cucumber, chopped celery, apple, parsley or water chestnuts.
Use meats that are sliced very thin; this will spread them out to look like a larger portion.
Use bread that is more thickly sliced, and consider more flavorful breads such as sour dough or rye bread.
Soups
Use lower-protein foods such as rice and pasta to add bulk to a soup without adding much protein.
Use milk substitutes that are low in protein when making cream soups.
Main Dishes
Use vegetables and grains as the main dish and meats or other high-value protein as the side dish.
Try kebabs, using smaller pieces of meats and more vegetables or fruits.
Prepare dishes with small pieces of meat or chicken mixed in with rice or pasta. Fried rice dishes or ground meat with pasta work well.
Toss together a chef salad with lettuce and crisp vegetables, adding smaller strips of meat and egg.
For casseroles, use smaller amounts of meat than the recipe calls for, increase the starch (rice or pasta). Buy low-sodium soups to use in all casserole recipes.
Allow yourself extra portions or larger servings of bread, rolls, pasta and rice to help meet your calorie needs without increasing your protein intake by very much.
For a stronger cheese taste with a smaller amount of cheese, buy sharp cheddar, Parmesan or Romano cheese. A little bit of these cheeses will go a long way.
What are calorie boosters?When you are eating less protein, you may also eat less calories. Using less calories may cause you to lose weight. It is always important for you to stay at your healthiest weight for your body size. To keep from losing too much weight, you can "make up" some of the calories lost when cutting down on protein foods by using foods with higher calorie levels.
Heart-healthy fats such as canola oil, olive oil corn oil, safflower oil, soybean oil or sunflower oil and mayonnaise-type salad dressings can be used in larger amounts to fry or season foods.
Candies such as hard candies, gum drops, jelly beans, chewy fruit flavored candies and marshmallows can be used as desserts or snacks. Sweeteners such as honey, jams or jellies and white sugar can be added to foods or drinks to increase calories. (Please consult your dietitian if you are diabetic.)
Click here for Modifying recipes to lower protein
http://www.kidney.org/news/newsroom/fsitem.cfm?id=24
If you have just learned that you have chronic kidney disease (CKD), your doctor may tell you to start limiting the protein in your diet. Changing your diet to meet your body's lower protein needs and still using the foods and recipes you are used to can be difficult. This fact sheet has ideas and tips to help you lower the protein in your favorite recipes, using the foods you normally use every day.
Why do I need to eat less protein?Protein is needed for growth, upkeep and repair of all parts of your body. Protein is found in almost all foods. When your body breaks down and uses the food you eat, a waste product called urea is made. When your kidneys are not working well, urea is not removed as it should be. Urea then builds up inside your body. Side effects of a high urea level are fatigue (tiredness) and poor appetite. By decreasing the amount of protein you eat, you can help your kidneys have a lighter work load, with less urea to clean out.
What foods have the most protein?There are two types of protein in the food we eat:
Animal protein is called high-value protein. It is easier for your body to use. Examples of high-value animal proteins are: red meat, chicken, turkey, pork, eggs and dairy products.* It is very important for you to eat enough high-value protein to keep your body healthy.* Dairy products are high-value protein, but are also high in phosphorus. You may need to use less dairy products in your diet to control your blood level of phosphorus.
Vegetable or plant proteins are low-value proteins. Examples of low-value proteins are: bread, cereals, dried beans, nuts, rice, pasta or noodles and vegetables.
A dietitian trained to work with those who have CKD can help you balance your protein.
How can I eat less protein and still feel like I am eating enough?Here are some tips to help you stretch protein foods so that a smaller amount will still feel like enough.
Sandwiches
Fill up sandwiches with lettuce, alfalfa sprouts, cucumber, chopped celery, apple, parsley or water chestnuts.
Use meats that are sliced very thin; this will spread them out to look like a larger portion.
Use bread that is more thickly sliced, and consider more flavorful breads such as sour dough or rye bread.
Soups
Use lower-protein foods such as rice and pasta to add bulk to a soup without adding much protein.
Use milk substitutes that are low in protein when making cream soups.
Main Dishes
Use vegetables and grains as the main dish and meats or other high-value protein as the side dish.
Try kebabs, using smaller pieces of meats and more vegetables or fruits.
Prepare dishes with small pieces of meat or chicken mixed in with rice or pasta. Fried rice dishes or ground meat with pasta work well.
Toss together a chef salad with lettuce and crisp vegetables, adding smaller strips of meat and egg.
For casseroles, use smaller amounts of meat than the recipe calls for, increase the starch (rice or pasta). Buy low-sodium soups to use in all casserole recipes.
Allow yourself extra portions or larger servings of bread, rolls, pasta and rice to help meet your calorie needs without increasing your protein intake by very much.
For a stronger cheese taste with a smaller amount of cheese, buy sharp cheddar, Parmesan or Romano cheese. A little bit of these cheeses will go a long way.
What are calorie boosters?When you are eating less protein, you may also eat less calories. Using less calories may cause you to lose weight. It is always important for you to stay at your healthiest weight for your body size. To keep from losing too much weight, you can "make up" some of the calories lost when cutting down on protein foods by using foods with higher calorie levels.
Heart-healthy fats such as canola oil, olive oil corn oil, safflower oil, soybean oil or sunflower oil and mayonnaise-type salad dressings can be used in larger amounts to fry or season foods.
Candies such as hard candies, gum drops, jelly beans, chewy fruit flavored candies and marshmallows can be used as desserts or snacks. Sweeteners such as honey, jams or jellies and white sugar can be added to foods or drinks to increase calories. (Please consult your dietitian if you are diabetic.)
Click here for Modifying recipes to lower protein
http://www.kidney.org/news/newsroom/fsitem.cfm?id=24
Transplant dilemma grows
By Barbara Feder Ostrov
San Jose Mercury News
(MCT)
SAN JOSE, Calif. - Their first meeting was as awkward as a blind date.
Herbert "Sonny" Davis needed a new kidney. Matt Thompson had one to give.
But first, they had to forge a friendship, or something like it.
Thompson learned about Davis' plight from a co-worker. But when he called Davis' transplant program to volunteer a kidney, a nurse turned him down flat: He couldn't donate to a man he had never met because the program simply wouldn't allow him to bear that risk for a stranger.
"Well, get to know him," another transplant employee advised Davis and his wife, Donne.
So began an unlikely friendship between Davis, a 65-year-old Jewish physicist from Menlo Park, Calif., and Thompson, a born-again Christian young enough to be his son. Ultimately, their bond satisfied Davis' transplant surgeons. Both men are recovering after their Nov. 14 operations at University of California-San Francisco.
Their story has a happy ending. But it highlights serious ethical questions about the changing world of organ donation, as living donors become more common, and patients increasingly go online to find the organs the medical system can't provide.
Medicine's "do no harm" principle requires doctors to justify performing risky surgery on a healthy donor. The closer the relationship, "the more medicine feels comfortable saying, `We'll subject you to risk,'" said University of Pennsylvania bioethicist Arthur Caplan.
But what is an acceptable relationship between donor and patient, and who defines it? Is it ethical if some people "jump ahead" of other, sicker patients on organ waiting lists simply because they are able to find a donor?
Some transplant programs do allow strangers to donate organs after rigorous medical and psychiatric screenings. Others, however, restrict donations to family and close friends, relying on a proven bond to justify the risk. Strangers too, they worry, might have mental problems or might be secretly paid, which is illegal in the United States.
"Kidney donation is not like giving blood," said Dr. John Scandling, medical director of the adult kidney and pancreas transplant program at Stanford University Medical Center. "It's major surgery. You can die."
Davis has lived with damaged kidneys for decades, the result of a childhood infection. He needed dialysis for four years before he received his first kidney transplant in 1995. He needed it again when that kidney failed nine years later.
His wife, Donne, who was not a compatible kidney match, begged for a donor in an emotional letter sent last summer to 140 friends and relatives. Davis, one of nearly 69,000 Americans needing a kidney transplant, faced up to six years on a waiting list.
The plea found its way to Thompson through Donne Davis' former boss at Foothill College, where she worked as an outreach counselor. The woman now works at the San Jose airport with Thompson, a security employee.
Thompson, who once worked as a missionary in Brazil, said he knew the letter was meant for him.
"I felt that God was compelling me to help out," Thompson said. "It was very frustrating, just wanting to help right away, but I couldn't."
Davis and Thompson knew they had to forge a bond that would assure Davis' surgeons that Thompson was donating his kidney for the right reasons. But where to start?
The Davises visited Thompson at his San Jose apartment, where they met his wife, Brenda, and his infant daughter, Grace, ate dinner, and played a board game. It was uncomfortable for everyone, as if they were trying to "force a relationship," Thompson said.
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San Jose Mercury News
(MCT)
SAN JOSE, Calif. - Their first meeting was as awkward as a blind date.
Herbert "Sonny" Davis needed a new kidney. Matt Thompson had one to give.
But first, they had to forge a friendship, or something like it.
Thompson learned about Davis' plight from a co-worker. But when he called Davis' transplant program to volunteer a kidney, a nurse turned him down flat: He couldn't donate to a man he had never met because the program simply wouldn't allow him to bear that risk for a stranger.
"Well, get to know him," another transplant employee advised Davis and his wife, Donne.
So began an unlikely friendship between Davis, a 65-year-old Jewish physicist from Menlo Park, Calif., and Thompson, a born-again Christian young enough to be his son. Ultimately, their bond satisfied Davis' transplant surgeons. Both men are recovering after their Nov. 14 operations at University of California-San Francisco.
Their story has a happy ending. But it highlights serious ethical questions about the changing world of organ donation, as living donors become more common, and patients increasingly go online to find the organs the medical system can't provide.
Medicine's "do no harm" principle requires doctors to justify performing risky surgery on a healthy donor. The closer the relationship, "the more medicine feels comfortable saying, `We'll subject you to risk,'" said University of Pennsylvania bioethicist Arthur Caplan.
But what is an acceptable relationship between donor and patient, and who defines it? Is it ethical if some people "jump ahead" of other, sicker patients on organ waiting lists simply because they are able to find a donor?
Some transplant programs do allow strangers to donate organs after rigorous medical and psychiatric screenings. Others, however, restrict donations to family and close friends, relying on a proven bond to justify the risk. Strangers too, they worry, might have mental problems or might be secretly paid, which is illegal in the United States.
"Kidney donation is not like giving blood," said Dr. John Scandling, medical director of the adult kidney and pancreas transplant program at Stanford University Medical Center. "It's major surgery. You can die."
Davis has lived with damaged kidneys for decades, the result of a childhood infection. He needed dialysis for four years before he received his first kidney transplant in 1995. He needed it again when that kidney failed nine years later.
His wife, Donne, who was not a compatible kidney match, begged for a donor in an emotional letter sent last summer to 140 friends and relatives. Davis, one of nearly 69,000 Americans needing a kidney transplant, faced up to six years on a waiting list.
The plea found its way to Thompson through Donne Davis' former boss at Foothill College, where she worked as an outreach counselor. The woman now works at the San Jose airport with Thompson, a security employee.
Thompson, who once worked as a missionary in Brazil, said he knew the letter was meant for him.
"I felt that God was compelling me to help out," Thompson said. "It was very frustrating, just wanting to help right away, but I couldn't."
Davis and Thompson knew they had to forge a bond that would assure Davis' surgeons that Thompson was donating his kidney for the right reasons. But where to start?
The Davises visited Thompson at his San Jose apartment, where they met his wife, Brenda, and his infant daughter, Grace, ate dinner, and played a board game. It was uncomfortable for everyone, as if they were trying to "force a relationship," Thompson said.
Read More
Wednesday, December 06, 2006
Caffeine Concerns for PKD Patients: 'Decaffeinated' Coffee May Be Anything But
By Neil Osterweil, Senior Associate Editor, MedPage Today Reviewed by Zalman S. Agus, MD; Emeritus Professor at the University of Pennsylvania School of Medicine. Caffeine-averse patients who think they're getting a free ride by drinking decaf at Starbucks, for instance, should know that it may be laden with the stimulant, claims not withstanding. Allegedly decaffeinated coffee served at various outlets contained enough caffeine in just two cups to equal levels of the stimulant found in a Coke or Pepsi, reported Bruce Goldberger, Ph.D., of the University of Florida here, and colleagues. Those who consume multiple cups of purportedly caffeine-free java should be aware that their cumulative daily consumption could easily add up to 85 mg of caffeine, the dose found in an average cup of the real stuff, the authors warned in the October issue of the Journal of Analytical Toxicity."The finding that decaffeinated coffee contains caffeine has far-reaching clinical consequences," the authors wrote. "Clinicians and patients should be aware that decaffeinated coffee frequently contains caffeine. Ingestion of multiple servings of decaffeinated beverages could result in caffeine doses equivalent to a caffeinated beverage. In addition, one must be mindful of the potential for pharmacological interactions that exist between caffeine and prescription medications." So-called decaf coffee may also contain just enough of the psychostimulant to foster dependence in caffeine-sensitive people, the authors suggested. "One has to wonder if decaf coffee has enough, just enough, caffeine to stimulate its own taking," said co-author Mark S. Gold, M.D. "Certainly, large cups and frequent cups of decaf would be expected to promote dependence and should be contraindicated in those whose doctors suggested caffeine-free diets." In addition to fending off fatigue and sharpening mental acuity, caffeine can increase heart rate, blood pressure, agitation, and anxiety in susceptible individuals. The FDA suggests that people on bronchodilators, anti-anxiety agents, and quinolone antibiotics lay-off caffeine. The stimulant is also contraindicated in patients with autosomal dominant polycystic kidney disease, because it promotes cyst enlargement, Dr. Goldberger and colleagues noted. To see whether there was more to decaffeinated coffee than meets the eye, the authors conducted a small two-part study. With the aid of a chemical testing lab in Severna Park, Md., the authors collected decaf coffee samples from 10 different specialty coffee shops, doughnut shops, fast food outlets, and an instant coffee brand from locations in Severna Park and Bethesda, Md., and Gainesville, Fla. They then collected decaffeinated espresso and decaffeinated standard coffee samples from a single outlet of Starbucks. They found that the 10 decaf samples initially collected contained caffeine ranging from 0 mg (Folger's instant decaf coffee crystals) to 13.9 mg/16 ounce servings (from Krispy Kreme, the doughnut chain). In contrast, caffeinated carbonated sodas contain about 18 mg to 48 mg of caffeine per 12-ounce serving. The authors then turned their attention to the Starbucks samples. They found that the decaf specialty drinks (latte, cappuccino, etc.) containing one 1 oz shot of "decaf" espresso contained between 3.0 and 15.8 mgs of caffeine. For these six samples, the intra-assay mean was 7.0 + 5.7 mg/serving (81.5% coefficient of variation). The brewed standard decaffeinated coffees, purchased at the same Starbucks on the following day, contained caffeine ranging from 12.0 mg to 13.4 mg per 16-ounce ("grande" or medium-size) serving. For the six samples, the intra-assay mean level of caffeine was 12.9 mg + 0.6 /16 oz. (4.4% coefficient of variation). "Carefully controlled studies show that caffeine doses as low as about 10 milligrams can produce reliable subjective and behavioral effects in sensitive individuals," commented Roland Griffiths, Ph.D., of Johns Hopkins, who researches the effects of caffeine in humans, but was not involved in the study. "More than 30% can discriminate the subjective effects of 18 mg or less. The present study shows that many decaffeinated coffee drinks deliver caffeine at doses above these levels." "The important point is that decaffeinated is not the same as caffeine-free," Dr. Griffiths said.
http://www.pkdcure.org/site/PageServer?pagename=medical06_caffine
http://www.pkdcure.org/site/PageServer?pagename=medical06_caffine
Pax2 gene dosage influences cystogenesis in autosomal dominant polycystic kidney disease.
Stayner C,
Iglesias DM,
Goodyer PR,
Ellis L,
Germino G,
Zhou J,
Eccles MR.
Mutations in PKD1 cause dominant polycystic kidney disease (PKD), characterized by large fluid-filled kidney cysts in adult life, but the molecular mechanism of cystogenesis remains obscure. Ostrom et al. [Dev. Biol., 219, 250-258 (2000)] showed that reduced dosage of Pax2 caused increased apoptosis, and ameliorated cystogenesis in Cpk mutant mice with recessive PKD. Pax2 is expressed in condensing metanephrogenic mesenchyme and arborizing ureteric bud, and plays an important role in kidney development. Transient Pax2 expression during fetal kidney mesenchyme-to-epithelial transition, as well as in nascent tubules, is followed by marked down-regulation of Pax2 expression. Here, we show that in humans with PKD, as well as in Pkd1(del34/del34) mutant mice, Pax2 was expressed in cyst epithelial cells, and facilitated cyst growth in Pkd1(del34/del34) mutant mice. In Pkd1(del34/del34) mutant kidneys, the expression of Pax2 persisted in nascent collecting ducts. In contrast, homozygous Pkd1(del34/del34) fetal mice carrying mutant Pax2 exhibited ameliorated cyst growth, although reduced cystogenesis was not associated with increased apoptosis. Pax2 expression was attenuated in nascent collecting ducts and absent from remnant cysts of Pkd1(del34/del34)/Pax2(1Neu/+) mutant mice. To investigate whether the Pkd1 gene product, Polycystin-1, regulates Pax2, MDCK cells were engineered constitutively expressing wild-type Pkd1; Pax2 protein levels and promoter activity were both repressed in MDCK cells over-expressing Pkd1, but not in cells without transgenic Pkd1. These data suggest that polycystin-1-deficient tubular epithelia persistently express Pax2 in ADPKD, and that Pax2 or its pathway may be an appropriate target for the development of novel therapies for ADPKD.
PMID: 17082250 [PubMed - in process]
Hum Mol Genet. 2006 Dec 15;15(24):3520-8. Epub 2006 Nov 2.
Iglesias DM,
Goodyer PR,
Ellis L,
Germino G,
Zhou J,
Eccles MR.
Mutations in PKD1 cause dominant polycystic kidney disease (PKD), characterized by large fluid-filled kidney cysts in adult life, but the molecular mechanism of cystogenesis remains obscure. Ostrom et al. [Dev. Biol., 219, 250-258 (2000)] showed that reduced dosage of Pax2 caused increased apoptosis, and ameliorated cystogenesis in Cpk mutant mice with recessive PKD. Pax2 is expressed in condensing metanephrogenic mesenchyme and arborizing ureteric bud, and plays an important role in kidney development. Transient Pax2 expression during fetal kidney mesenchyme-to-epithelial transition, as well as in nascent tubules, is followed by marked down-regulation of Pax2 expression. Here, we show that in humans with PKD, as well as in Pkd1(del34/del34) mutant mice, Pax2 was expressed in cyst epithelial cells, and facilitated cyst growth in Pkd1(del34/del34) mutant mice. In Pkd1(del34/del34) mutant kidneys, the expression of Pax2 persisted in nascent collecting ducts. In contrast, homozygous Pkd1(del34/del34) fetal mice carrying mutant Pax2 exhibited ameliorated cyst growth, although reduced cystogenesis was not associated with increased apoptosis. Pax2 expression was attenuated in nascent collecting ducts and absent from remnant cysts of Pkd1(del34/del34)/Pax2(1Neu/+) mutant mice. To investigate whether the Pkd1 gene product, Polycystin-1, regulates Pax2, MDCK cells were engineered constitutively expressing wild-type Pkd1; Pax2 protein levels and promoter activity were both repressed in MDCK cells over-expressing Pkd1, but not in cells without transgenic Pkd1. These data suggest that polycystin-1-deficient tubular epithelia persistently express Pax2 in ADPKD, and that Pax2 or its pathway may be an appropriate target for the development of novel therapies for ADPKD.
PMID: 17082250 [PubMed - in process]
Hum Mol Genet. 2006 Dec 15;15(24):3520-8. Epub 2006 Nov 2.
Aquaporins: a promising target for drug development.
Jeyaseelan K,
Sepramaniam S,
Armugam A,
Wintour EM.
Yong Loo Lin School of Medicine, National University of Singapore, Department of Biochemistry, 8 Medical Drive, 117597, Singapore. bchjeya@nus.edu.sg
Aquaporins (AQPs) are a family of small hydrophobic, integral membrane proteins that are expressed in all living organisms and play critical roles in controlling the water flow into and out of cells. So far, 13 different AQPs have been identified in mammals (AQP 0-12). AQPs have recently been implicated in various diseases such as cancer, cataract, brain oedema, gallstone disease and nephrogenic diabetes insipidus, as well as in the development of obesity and polycystic kidney disease. Interfering with the expression of AQPs will undoubtedly have therapeutic applications. Hence, in this review, the authors look at each AQP and its association with various pathological conditions in humans and demonstrate that they form potential targets for the treatment of such diseases.
PMID: 17105375 [PubMed - in process]
Expert Opin Ther Targets. 2006 Dec;10(6):889-909
Sepramaniam S,
Armugam A,
Wintour EM.
Yong Loo Lin School of Medicine, National University of Singapore, Department of Biochemistry, 8 Medical Drive, 117597, Singapore. bchjeya@nus.edu.sg
Aquaporins (AQPs) are a family of small hydrophobic, integral membrane proteins that are expressed in all living organisms and play critical roles in controlling the water flow into and out of cells. So far, 13 different AQPs have been identified in mammals (AQP 0-12). AQPs have recently been implicated in various diseases such as cancer, cataract, brain oedema, gallstone disease and nephrogenic diabetes insipidus, as well as in the development of obesity and polycystic kidney disease. Interfering with the expression of AQPs will undoubtedly have therapeutic applications. Hence, in this review, the authors look at each AQP and its association with various pathological conditions in humans and demonstrate that they form potential targets for the treatment of such diseases.
PMID: 17105375 [PubMed - in process]
Expert Opin Ther Targets. 2006 Dec;10(6):889-909
PKD Blog News
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Monday, December 04, 2006
Learn More About PKD Clinical Trials
(Updated October 11, 2006)Tolvaptan and HALT PKD clinical trials are enrolling patients, while promising new research on drugs such as rapamycin are already leading to additional studies. Read below for more information or, to visit the Current Research section of the website, click here.
* NOTE: Each trial is different and demands on patients vary widely. Before signing up for any clinical trials, talk to your doctor or health care team. To learn more about the clinical trial process and how drug therapies are approved through the U.S. Food and Drug Administration, please click here.
Current Clinical Trials
Rapamune (Sirolimus/Rapamycin) This is a 24-month prospective, controlled open label study at the University of Zurich in Switzerland, investigating whether Rapamycin retards cyst growth and slows renal functional deterioration in patients with PKD. Renal volume will be measured by magnetic resonance imaging. More information about the study and eligibility criteria can be obtained by clicking here, or you may directly email Dr. Andreas Serra, Principal Investigator, at andreas.serra@usz.ch
CRISP IIThe CRISP study has been selected for extended funding which should begin in the next three months. This continuation of the original CRISP study, now called CRISP II, will follow the original patient cohort for an additional four years to study the relationship between kidney size and disease progression. Some patients may be in other studies as well but will continue to be monitored here. To read about the original CRISP study, click here.Tolvaptan (Otsuka Maryland Research Institute): This study, which recently received “fast track” designation by the Food and Drug Administration because of its promise as a treatment for PKD, is looking at the effectiveness of a vasopressin antagonist drug to slow or stop cyst growth in PKD patients. Phase II clinical trials are finishing up. Enrollment has not yet begun for Phase III clinical trials. Phase III trials are larger studies looking at drug effectiveness in PKD patients living in the Americas, Asia, and Europe. Patients and physicians interested in participating in these trials should contact Otsuka at 866-712-5837. Information on Otsuka can be obtained from their public website at http://www.otsuka.com/ .
HALT PKD Treatment Network (NIDDK): The HALT study is a nationwide research initiative to investigate the effectiveness of anti-hypertensive drugs on PKD progression and its cardiovascular complications. ACE (angiotensin converting enzyme) inhibitors in combination with or without ARB (angiotensin receptor binding) inhibitors will be evaluated. The study will involve travel to selected sites for periodic examinations, home blood pressure monitoring and laboratory testing. Costs for medications, home blood pressure equipment and patient evaluations will be fully covered. Travel costs will be totally or partially covered, depending on how far the participant lives from the study site. Enrolment begins Spring 2006. For more information about the study, go to www.clinicaltrials.gov/ct/ and type in “polycystic kidney disease” and select “HALT Progression of PKD” or call the study sites listed below:
- Tufts-New England Medical Center in Boston, MA: 1-866-846-2735 or 1-617-636-8783- Beth Israel Deaconess Medical Center in Boston, MA: 1-617-636-8783 or 1-866-650-1815 - Emory University in Atlanta, GA: 1-404-686-8280.- Mayo Clinic in Rochester, MN: 1-507-284-0944 or 1-888-630-2616- University of Colorado in Denver, CO: 1-877-765-9297- Kansas University Medical Center in Kansas City, KS: 1-913-588-7609- Cleveland Clinic Foundation in Cleveland, OH: 1-800-223-2273, ext 44680Heart Disease and PKD: The aim of this non-invasive study is to examine possible mechanisms leading to heart disease in PKD. The study is located at the Tufts-New England Medical Center and is directed to PKD patients in the Boston area. Those interested in participating, call Vandana Menon, M.D., Ph.D. at (617) 636-8791 or (617) 636-5895.ARPKD and Congenital Hepatic Fibrosis: The National Human Genome Research Institute at the National Institutes of Health wants to collect comprehensive date on kidney and liver disease in ARPKD/CHF and follow patients over time to provide the groundwork for more focused studies and novel therapeutic interventions. The protocol includes children and adults with a clinical diagnosis of ARPKD/CHF. Patients who have received a kidney or liver transplant and have stable graft function without severe complications are eligible. The study requires admission to the NIH Clinical Center for 4-5 days, with follow-up visits every 1-2 years. There are no medical expenses for the patients, and travel can be provided. For more information, contact Dr. Meral Gunay at 1-301-594-4181 or by e-mail at mgaygun@nih.gov or go to www.clinicaltrials.gov/ct/ and type in “polycystic kidney disease” and select “Evaluation of ARPKD and Congenital Hepatic Fibrosis.”
Future Clinical Trials
Rapamune (Sirolimus/Rapamycin) This study is a prospective, randomized, placebo-controlled clinical trial sponsored by the Cleveland Clinic and designed to evaluate the effects of an agent (rapamycin) that has antiproliferative, antiangiogenesis and tumor-progression blocking capabilities. This study is not yet open for patient recruitment. For more information, go to www.clinicaltrials.gov/ct/ and type in “polycystic kidney disease” and select “Pilot Study of Rapamycin as Treatment for Autosomal Dominant PKD.” The person to contact for more information is Susan Wirth, BSN, at wirths@ccf.org.
Statin Therapy and PKD Disease Progression in Children and Young AdultsThe purpose of this clinical trial is to determine the effect of blood pressure control with angiotensin converting enzyme (ACE) inhibition on renal cyst growth over a five-year study period in children and young adults aged 4-21 years with ADPKD. Results of this study could significantly impact the standard of care for management of ADPKD in this population. The study will take place at The Children’s Hospital in Denver, CO. All expenses including study-related medications, a home blood pressure machine, travel costs to and from Denver (including one parent to accompany minor children) and lab and radiology testing will be provided. For more information, call Dr. Melissa Cadnapaphornchai toll-free at 877.765.9297 or send an e-mail to pkd.nurse@uchsc.edu .Observational StudyChronic Kidney Disease in Children Prospective Cohort Study (CKiD)This is a prospective epidemiological study of children with chronic kidney disease and includes children with ARPKD and ADPKD. The primary goals of the study are to determine the risk factors for decline in kidney function and define how a progressive decline in kidney function impacts neurocognitive function and behavior; the risk factors for cardiovascular disease; and growth failure and its associated morbidity. Enrollment has begun. For more information go to http://www.clinicaltrials.gov/ct/show/NCT00327860.
Study sites and contact information are as follows: 1. Johns Hopkins University, Baltimore, MD: Susan Furth, M.D., Ph.D., sfurth@jhmi.edu or 410-502-7964 2. Children’s Mercy Hospital, Kansas City, MO: Brad Warady, M.D., bwarady@cmh.edu or 816-234-3812Somatostatin This general aim of this study is to compare the effects on disease progression of three year treatment regimen using long-acting somatostatin or placebo in patients with ADPKD and normal renal function or mild to moderate renal insufficiency. This study is sponsored by the Mario Negri Institute for Pharmacological Research in Bergamo, Italy. This study is not yet open for patient recruitment. For more information, go to www.clinicaltrials.gov/ct/ and type in “polycystic kidney disease”. Then select “Somatostatin in Polycystic Kidney: A Long-Term Three Year Follow-up Study” or contact Norberto Perico, M.D., at perico@marionegri.it . PKD Gene Modifier Mapping Study (Canadian Institutes of Health Research): This is an international observational study designed to map modifier genes for renal disease progression in type I ADPKD. There are 10 different ADPKD research centers in North America and Europe.
http://www.pkdcure.org/site/PageServer?pagename=mn_Aprilclinicaltrials
* NOTE: Each trial is different and demands on patients vary widely. Before signing up for any clinical trials, talk to your doctor or health care team. To learn more about the clinical trial process and how drug therapies are approved through the U.S. Food and Drug Administration, please click here.
Current Clinical Trials
Rapamune (Sirolimus/Rapamycin) This is a 24-month prospective, controlled open label study at the University of Zurich in Switzerland, investigating whether Rapamycin retards cyst growth and slows renal functional deterioration in patients with PKD. Renal volume will be measured by magnetic resonance imaging. More information about the study and eligibility criteria can be obtained by clicking here, or you may directly email Dr. Andreas Serra, Principal Investigator, at andreas.serra@usz.ch
CRISP IIThe CRISP study has been selected for extended funding which should begin in the next three months. This continuation of the original CRISP study, now called CRISP II, will follow the original patient cohort for an additional four years to study the relationship between kidney size and disease progression. Some patients may be in other studies as well but will continue to be monitored here. To read about the original CRISP study, click here.Tolvaptan (Otsuka Maryland Research Institute): This study, which recently received “fast track” designation by the Food and Drug Administration because of its promise as a treatment for PKD, is looking at the effectiveness of a vasopressin antagonist drug to slow or stop cyst growth in PKD patients. Phase II clinical trials are finishing up. Enrollment has not yet begun for Phase III clinical trials. Phase III trials are larger studies looking at drug effectiveness in PKD patients living in the Americas, Asia, and Europe. Patients and physicians interested in participating in these trials should contact Otsuka at 866-712-5837. Information on Otsuka can be obtained from their public website at http://www.otsuka.com/ .
HALT PKD Treatment Network (NIDDK): The HALT study is a nationwide research initiative to investigate the effectiveness of anti-hypertensive drugs on PKD progression and its cardiovascular complications. ACE (angiotensin converting enzyme) inhibitors in combination with or without ARB (angiotensin receptor binding) inhibitors will be evaluated. The study will involve travel to selected sites for periodic examinations, home blood pressure monitoring and laboratory testing. Costs for medications, home blood pressure equipment and patient evaluations will be fully covered. Travel costs will be totally or partially covered, depending on how far the participant lives from the study site. Enrolment begins Spring 2006. For more information about the study, go to www.clinicaltrials.gov/ct/ and type in “polycystic kidney disease” and select “HALT Progression of PKD” or call the study sites listed below:
- Tufts-New England Medical Center in Boston, MA: 1-866-846-2735 or 1-617-636-8783- Beth Israel Deaconess Medical Center in Boston, MA: 1-617-636-8783 or 1-866-650-1815 - Emory University in Atlanta, GA: 1-404-686-8280.- Mayo Clinic in Rochester, MN: 1-507-284-0944 or 1-888-630-2616- University of Colorado in Denver, CO: 1-877-765-9297- Kansas University Medical Center in Kansas City, KS: 1-913-588-7609- Cleveland Clinic Foundation in Cleveland, OH: 1-800-223-2273, ext 44680Heart Disease and PKD: The aim of this non-invasive study is to examine possible mechanisms leading to heart disease in PKD. The study is located at the Tufts-New England Medical Center and is directed to PKD patients in the Boston area. Those interested in participating, call Vandana Menon, M.D., Ph.D. at (617) 636-8791 or (617) 636-5895.ARPKD and Congenital Hepatic Fibrosis: The National Human Genome Research Institute at the National Institutes of Health wants to collect comprehensive date on kidney and liver disease in ARPKD/CHF and follow patients over time to provide the groundwork for more focused studies and novel therapeutic interventions. The protocol includes children and adults with a clinical diagnosis of ARPKD/CHF. Patients who have received a kidney or liver transplant and have stable graft function without severe complications are eligible. The study requires admission to the NIH Clinical Center for 4-5 days, with follow-up visits every 1-2 years. There are no medical expenses for the patients, and travel can be provided. For more information, contact Dr. Meral Gunay at 1-301-594-4181 or by e-mail at mgaygun@nih.gov or go to www.clinicaltrials.gov/ct/ and type in “polycystic kidney disease” and select “Evaluation of ARPKD and Congenital Hepatic Fibrosis.”
Future Clinical Trials
Rapamune (Sirolimus/Rapamycin) This study is a prospective, randomized, placebo-controlled clinical trial sponsored by the Cleveland Clinic and designed to evaluate the effects of an agent (rapamycin) that has antiproliferative, antiangiogenesis and tumor-progression blocking capabilities. This study is not yet open for patient recruitment. For more information, go to www.clinicaltrials.gov/ct/ and type in “polycystic kidney disease” and select “Pilot Study of Rapamycin as Treatment for Autosomal Dominant PKD.” The person to contact for more information is Susan Wirth, BSN, at wirths@ccf.org.
Statin Therapy and PKD Disease Progression in Children and Young AdultsThe purpose of this clinical trial is to determine the effect of blood pressure control with angiotensin converting enzyme (ACE) inhibition on renal cyst growth over a five-year study period in children and young adults aged 4-21 years with ADPKD. Results of this study could significantly impact the standard of care for management of ADPKD in this population. The study will take place at The Children’s Hospital in Denver, CO. All expenses including study-related medications, a home blood pressure machine, travel costs to and from Denver (including one parent to accompany minor children) and lab and radiology testing will be provided. For more information, call Dr. Melissa Cadnapaphornchai toll-free at 877.765.9297 or send an e-mail to pkd.nurse@uchsc.edu .Observational StudyChronic Kidney Disease in Children Prospective Cohort Study (CKiD)This is a prospective epidemiological study of children with chronic kidney disease and includes children with ARPKD and ADPKD. The primary goals of the study are to determine the risk factors for decline in kidney function and define how a progressive decline in kidney function impacts neurocognitive function and behavior; the risk factors for cardiovascular disease; and growth failure and its associated morbidity. Enrollment has begun. For more information go to http://www.clinicaltrials.gov/ct/show/NCT00327860.
Study sites and contact information are as follows: 1. Johns Hopkins University, Baltimore, MD: Susan Furth, M.D., Ph.D., sfurth@jhmi.edu or 410-502-7964 2. Children’s Mercy Hospital, Kansas City, MO: Brad Warady, M.D., bwarady@cmh.edu or 816-234-3812Somatostatin This general aim of this study is to compare the effects on disease progression of three year treatment regimen using long-acting somatostatin or placebo in patients with ADPKD and normal renal function or mild to moderate renal insufficiency. This study is sponsored by the Mario Negri Institute for Pharmacological Research in Bergamo, Italy. This study is not yet open for patient recruitment. For more information, go to www.clinicaltrials.gov/ct/ and type in “polycystic kidney disease”. Then select “Somatostatin in Polycystic Kidney: A Long-Term Three Year Follow-up Study” or contact Norberto Perico, M.D., at perico@marionegri.it . PKD Gene Modifier Mapping Study (Canadian Institutes of Health Research): This is an international observational study designed to map modifier genes for renal disease progression in type I ADPKD. There are 10 different ADPKD research centers in North America and Europe.
http://www.pkdcure.org/site/PageServer?pagename=mn_Aprilclinicaltrials
Saturday, December 02, 2006
Learn More About PKD Clinical Trials
(Updated October 11, 2006)
Tolvaptan and HALT PKD clinical trials are enrolling patients, while promising new research on drugs such as rapamycin are already leading to additional studies. Read below for more information or, to visit the Current Research section of the website, click here.
* NOTE: Each trial is different and demands on patients vary widely. Before signing up for any clinical trials, talk to your doctor or health care team. To learn more about the clinical trial process and how drug therapies are approved through the U.S. Food and Drug Administration, please click here.
Source:
http://www.pkdcure.org/site/PageServer?pagename=mn_Aprilclinicaltrials
Tolvaptan and HALT PKD clinical trials are enrolling patients, while promising new research on drugs such as rapamycin are already leading to additional studies. Read below for more information or, to visit the Current Research section of the website, click here.
* NOTE: Each trial is different and demands on patients vary widely. Before signing up for any clinical trials, talk to your doctor or health care team. To learn more about the clinical trial process and how drug therapies are approved through the U.S. Food and Drug Administration, please click here.
Source:
http://www.pkdcure.org/site/PageServer?pagename=mn_Aprilclinicaltrials
Friday, December 01, 2006
Cancer Drug Has Promise In Kidney Disease, ArthritisBioWorld
Today - Nov. 30, 2006
Recyclacelled Compound
Polycystic kidney disease strikes in varying severity. But in bad cases, the normally fist-sized kidney ?can reach the size of a football,? Katharine Klinger, senior vice president of genetics at Framingham, Mass.-based Genzyme Inc., told BioWorld Today.
The cause of the disorder is clear: It?s a genetic disease in which either polycystin-1 or polycystin-2 are mutated. That in turn leads cysts to replace nephrons, the filtering units of the kidneys. Aside from the fluid buildup, that prevents the kidneys from filtering waste.
The cure is less clear. ?Right now, there is no therapy for ...
To continue reading the complete article, login or registerbelow and get free instant access.
http://www.therapeuticsdaily.com/news/article.cfm?contenttype=sentryarticle&contentvalue=1165305&channelID=29
Recyclacelled Compound
Polycystic kidney disease strikes in varying severity. But in bad cases, the normally fist-sized kidney ?can reach the size of a football,? Katharine Klinger, senior vice president of genetics at Framingham, Mass.-based Genzyme Inc., told BioWorld Today.
The cause of the disorder is clear: It?s a genetic disease in which either polycystin-1 or polycystin-2 are mutated. That in turn leads cysts to replace nephrons, the filtering units of the kidneys. Aside from the fluid buildup, that prevents the kidneys from filtering waste.
The cure is less clear. ?Right now, there is no therapy for ...
To continue reading the complete article, login or registerbelow and get free instant access.
http://www.therapeuticsdaily.com/news/article.cfm?contenttype=sentryarticle&contentvalue=1165305&channelID=29
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