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Polycystic Kidney: more books (43)

Polycystic kidney disease: Etiology, pathogenesis, and treatment by John R Martinez, 1995
Problems in Diagnosis and Management of Polycystic Kidney Disease: Proceedings o by Jared J.; Gardner, Kenneth D.; PKR Foundation Grantham, 1985-01-01
Bilateral polycystic disease of the kidneys;: A follow-up of two hundred and eighty-four patiets [sic] and their families (Acta medica Scandinavica. Supplementum) by O. Z Dalgaard, 1957
Problems in Diagnosis and Management of Polycystic Kidney Disease: Proceedings o
Polycystic Kidney Disease (Contributions to Nephrology) by M. H.; Devoto, M. Breuning,
Arterial supply of the congenital polycystic kidney and its relation to the clinical picture by Saul A Ritter, 1929
Experimental infantile polycystic kidney in rats: The influence of age and sex by J. E. M McGeoch, 1972
Remarks on the diagnosis of polycystic kidney by William Osler, 1915
Comparative study of circulatory changes in hydronephrosis, caseo-cavernous tuberculosis, and polycystic kidney: A preliminary report by Frank Hinman, 1924
Autosomal dominant polycystic kidney disease: a case study.(Continuing Nursing Education)(Case study): An article from: Nephrology Nursing Journal by Angela Phillips, 2009-01-01
Non-B DNA structure-induced genetic instability [An article from: Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis by G. Wang, K.M. Vasquez, 2006-06-25
Remembering Erma. (Erma Bombeck)(Obituary): An article from: Medical Update by Wendy R. Braun, 1996-09-01
To Live or Die in Arizona by Elizabeth Bruening Lewis, 2002-04
The Reluctant Donor by Suzanne Ruff, 2010-04-06

lists with details

KFOC - Polycystic Kidney Disease
Polycystic means many fluidfilled sacs or cysts . polycystic kidney disease (PKD) is a disease which causes cysts to form in the kidneys.
http://www.kidney.ca/english/publications/brochures/polycystic/polycystic.htm

Extractions: PKD is an inherited disease. This means that it is passed from parents to children. Every person has 23 different pairs of chromosomes, one set coming from each parent. The chromosomes are messengers which carry information in the form of genes. If you inherit the gene for PKD then you will either have the disease or you will be a silent carrier (where you don't have the disease but you may pass on the gene). This will depend on the type of PKD gene passed on to you.
Polycystic Kidney Disease
Detailed information on the different types of polycystic kidney disease, including autosomal dominant polycystic kidney disease, autosomal recessive
http://www.healthsystem.virginia.edu/uvahealth/adult_urology/polycyst.cfm

Extractions: [ Skip Navigation ] Topics All About Cancer Blood Disorders Bone Disorders Breast Health Cancer Cardiovascular Disease Dermatology Diabetes Digestive Disorders Endocrinology Environmental Medicine Eye Care Glossary Gynecological Health Infectious Diseases Kidney Disease Men's Health Mental Health Nervous System Disorders Non-Trauma Emergency Oral Health Orthopaedics Otolaryngology Pathology Pediatrics, General Health Prostate Health Radiology Respiratory Disorders Skin Cancer Surgical Care Urology Women's Health Search This Site Polycystic kidney disease (PKD) is a genetic disorder characterized by the growth of numerous cysts filled with fluid in the kidneys. PKD cysts can reduce kidney function, leading to kidney failure. PKD can also cause cysts in the liver and problems in other organs, such as the heart and blood vessels in the brain. PKD is the fourth leading cause of kidney failure and affects approximately 500,000 people in the US. According to the National Kidney Foundation, about 50 percent of people with autosomal dominant form of PKD progress to kidney failure, or end-stage renal disease (ESRD) by age 60 and about 60 percent will have kidney failure by age 70.
Polycystic Kidney Disease
Penn State Hershey Medical Center provides world class care and services to patients.
http://www.hmc.psu.edu/healthinfo/jkl/kidneydisease.htm
Polycystic Kidney Disease Chat & Community
Hi there! I have PKD and started this caring support group 5yrs ago. Being as we are a close group PLEASE use a first name and NOT a wierd or strange screen
http://communities.msn.com/PolycysticKidneydiseasechatcommunity/home.htm

Extractions: Chat Times Sunday,Tuesday,Thursday @9pm.EST Code of Conduct I will NOT tolerate for any reason the following No flamming of members No profanity EVER No dirty jokes allowed on boards or chat!! Also, please do NOT give out MEDICAL ADVICE . We are a SUPPORT GROUP only. We share our experiences, strenghts and hopes here. We are a family rated group. We invite your friends to join in and learn about PKD also. They are welcome to post and join us in our chat room. If you are interested in becoming a PKD Chapter Coordinator, please contact the PKD Foundation by email at WWW.PKDCURE.ORG We will be more than happy to talk to you about this great experience. Also, if you would like to make a monitary contribution to the PKD Foundation, you can do so by contacting them at WWW.PKDCURE.ORG You can call the PKD Foundation Toll Free at Our site managers are as follows: Please feel free to talk to these wonderful members at anytime.
THE MERCK MANUAL--SECOND HOME EDITION, Polycystic Kidney Disease In Ch. 146, Tub
polycystic kidney disease is a hereditary disorder in which many The genetic defect that causes polycystic kidney disease may be dominant or recessive.
http://www.merck.com/mmhe/sec11/ch146/ch146k.html

Extractions: var externalLinkWarning = "The link you have selected will take you to a site outside Merck and The Merck Manuals.*n*nThe Merck Manuals do not review or control the content of any non-Merck site. The Merck Manuals do not endorse and are not responsible for the accuracy, content, practices, or standards of any non-Merck sources."; Search The Second Home Edition , Online Version Search Index A B C D ... Z Sections Accidents and Injuries Blood Disorders Bone, Joint, and Muscle Disorders Brain, Spinal Cord, and Nerve Disorders ... Women's Health Issues Resources Anatomical Drawings Multimedia Pronunciations Weights and Measures ... , Online Version Section Kidney and Urinary Tract Disorders Chapter Tubular and Cystic Kidney Disorders Topics Introduction Alport's Syndrome Bartter's Syndrome Cystinuria ... Nephrogenic Diabetes Insipidus Polycystic Kidney Disease Renal Glucosuria Renal Tubular Acidosis Polycystic Kidney Disease Buy The Book Print This Topic Email This Topic Pronunciations aneurysm computed tomography cystinuria diabetes insipidus ... ultrasonography Polycystic kidney disease is a hereditary disorder in which many fluid-filled sacs (cysts) form in both kidneys; the kidneys grow larger but have less functioning kidney tissue. Multimedia Polycystic Kidney Disease The genetic defect that causes polycystic kidney disease may be dominant or recessive. That is, a person with the disease has inherited either one copy of a dominant gene from one parent or two copies of a recessive gene, one from each parent. Those with dominant gene inheritance usually have no symptoms until adulthood; those with recessive gene inheritance develop severe illness in childhood.
Polycysic Kidney Disease - Your Genes, Your Health - DNA Learning Center - Cold
In polycystic kidney disease (PKD), cysts grow inside a persons kidneys, A person who has a family history of polycystic kidney disease or who has
http://www.ygyh.org/pkd/description.html

Extractions: Fragile X Syndrome In polycystic kidney disease (PKD), cysts grow inside a persons kidneys, in most cases leading to kidney failure. A healthy kidney filters out toxins in the blood and eliminates them from the body in the form of urine. In autosomal dominant polycystic kidney disease (ADPKD), there are at least two genes, which, if mutated, can cause cysts to grow in the kidneys. These genes are PKD1 on chromosome 16 and PKD2 on chromosome 4. In autosomal dominant polycystic kidney disease (ADPKD), there are at least two genes, which, if mutated, can cause cysts to grow in the kidneys. These genes are PKD1 on chromosome 16 and PKD2 on chromosome 4. Everyone has two copies of both the PKD1 and PKD2 genes; one PKD1 and one PKD2 gene is inherited from each parent. A person with a mutation in one of the PKD1 or PKD2 genes will eventually develop polycystic kidney disease. There are no directly adverse consequences of having only one working copy of PKD1 or PKD2. However, over the years, there is a fairly high probability of "spontaneous" mutations in the working copies of PKD1 or PKD2. For a person who inherited a mutation in PKD1 or PKD2, every kidney cell has that mutation. Over the years, some fraction of the kidney cells may acquire a mutation in the other copy of the gene. Kidney cells with two mutated copies of the PKD1 or PKD2 genes will develop into cysts. Why are PKD1 and PKD2 so important? The cell uses these genes to produce two proteins, polycystin-1 and polycystin-2. Together, polycystin-1 and polycystin-2 form a channel on the surface of the cell, which allows small molecules to enter. These molecules "identify" the cell as a kidney cell and trigger the production of kidney structures. If polycystin-1 or polycystin-2 don't work, the cell does not get the signals that identify it as a kidney cell. No kidney structures are made. These undetermined cells do not have any blood-filtering abilities and grow into cysts in the kidneys. As the cysts grow, their size can also block the ability of neighboring kidney cells from filtering blood. Eventually, the entire kidney may fail, at which point the patient will require dialysis and a kidney transplant. A person who has a family history of polycystic kidney disease or who has cysts in the liver is at risk for having polycystic kidney disease. A doctor may be able to diagnose PKD by sight or touch. Large cysts in the kidneys can cause the abdomen to bulge. To confirm the diagnosis, the doctor will use some type of imaging technology to detect the cysts. Ultrasound is the most commonly used technology. An ultrasound machine uses the principle of echolocation to see inside the body. Sound waves radiate from the ultrasound probe and penetrate into the body. If they hit dense tissue, they are more likely to bounce back. The ultrasound probe is connected to a computer that calculates the distance the sound waves traveled before bouncing back. The number of waves that came back after a specific amount of time tells the computer how dense the tissue is at that distance into the body. The densities and distances are used to draw a picture. Ultrasound is the best way of diagnosing polycystic kidney disease if the cysts have already begun to grow. Genetic tests are sometimes used to identify PKD before cysts appear, but these tests are usually family-specific and can be expensive. Autosomal dominant polycystic kidney disease (ADPKD) is a dominant genetic disorder. That means you only need to inherit one mutation in one of the PKD genes to develop PKD. When each parent produces sperm or eggs, only one of their two PKD1 genes goes into each cell. In this case, the father has a mutated PKD gene; half of his sperm will have the mutated PKD gene. The child will inherit one copy of the PKD gene from the father and one from the mother. In this case, the child inherited the mutant PKD gene. He will develop autosomal dominant polycystic kidney disease just like his father. Autosomal dominant polycystic kidney disease can also occur as the result of a spontaneous mutation. If neither parent had the disease, but a PKD gene was mutated in the sperm or egg, you can still have the disease (about 10% of cases fall into this category). This child has one mutant copy of the PKD1 gene. He has autosomal dominant polycystic kidney disease. If you have autosomal dominant polycystic kidney disease (ADPKD) and your partner does not, each of your children has a 50% chance of having the desease. To see why, we first represent the parental genes with letters: big P represents the normal PKD1 gene, little p represents the mutant PKD1 gene. If you have autosomal dominant polycystic kidney disease (ADPKD) and your partner does not, each of your children has a 50% chance of having the desease. To see why, we first represent the parental genes with letters: big P represents the normal PKD1 gene, little p represents the mutant PKD1 gene. Again, we can count the squares to determine the probability of different outcomes if these parents have a child. There is still a 50% chance that each child will have polycystic kidney disease. However, there is an additional 25% chance of miscarriage. The most important thing to remember about these odds is that they apply to every child this couple has. It may be useful to think of the Punnett square as a roulette wheel. Each child is a separate "spin of the wheel", so each child has a 50% chance of having polycystic kidney disease. If you have autosomal recessive polycystic kidney disease (ARPKD) and your partner does not, your children cannot have the disease. To see why, we first represent the parental genes with letters: big P represents the normal ARPKD gene, little p represents the mutant ARPKD gene. Each parent donates one of their ARPKD genes to the child, so we place one of the father's genes and one of the mother's genes in each box. Each completed box shows a different possible combination of genes (a genotype) for the child, and the entire square shows all possible combinations. If you have autosomal recessive polycystic kidney disease and your partner is a carrier, your children have a 50% chance of having the disease. To see why, we will draw up a new square, with a Pp mother and a pp father. There are two basic forms of the disease: autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD). Both have generally the same clinical symptoms, but different underlying genetic causes. ADPKD is dominant; a person needs only inherit one copy of the mutated gene to develop the disease. ARPKD is recessive; a person needs to inherit two copies of the mutated gene, one from each parent, in order to develop the disease. People with polycystic kidney disease have multiple cysts in their kidneys. These cysts invariably increase the size of the kidneys squeezing on surrounding blood vessels. This often causes high blood pressure and impairs the kidney's ability to remove harmful toxins from the bloodstream. In a majority of cases, the kidneys fail. Cysts often appear in other parts of the body: liver, pancreas, seminal vesicles and ovaries. In many cases, the disease causes one of two forms of heart disease (left ventricular hypertrophy and mitral valve prolapse), intracranial aneurysms, abdominal hernias, and other less common symptom. Autosomal dominant polycystic kidney disease (ADPKD) has an incidence rate in the United States of 1 in 500 to 1 in 1,000. ADPKD is generally asymptomatic until the second or third decade of life. Autosomal recessive polycystic kidney disease (ARPKD) is less common, with an incidence rate of approximately 1 in 10,000. ARPKD affects infants, either in utero or in the neonatal stage and has a high rate of mortality. Polycystic kidney disease causes large cysts to grow in an affected person's kidneys. Ultrasound and other imaging technologies can be used to see the cysts and diagnose the disease. A genetic test may also be used in a family with a history of the disease. Autosomal dominant polycystic kidney disease (ADPKD) is caused by a mutation in one of two genes: PKD1, PKD2. Proteins encoded by these genes seem to work together as a signaling system for kidney cells. When this signaling system breaks down, the cells no longer develop into the correct kidney structures, and instead form amorphous cysts. There is currently no cure for polycystic kidney disease. In the early stages, a patient can be treated for high blood pressure, pain, and any other secondary symptoms. If the disease progresses to the point of kidney failure, dialysis and kidney transplantation provide replacement therapy, but does not cure PKD. Facts and theories symptoms treatment cause testing and screening incidenceA healthy kidney works just like a filter blood full of toxins is pumped into the kidney, the toxins are sent to the bladder, and then clean blood is pumped back out. When the kidneys fail, as can happen for people with polycystic kidney disease, toxins are no longer cleared from the blood. Dialysis works like an artificial kidney to filter toxins out of the blood. The first type of dialysis to be developed was hemodialysis. Blood is pumped out of the body into a machine, which filters the blood. The blood is then pumped back into the body. The part of the dialysis machine that does all of the work is called the dialyzer. Both blood and dialysate flow through this tube, separated by a thin membrane. Dialysate is a liquid that mimics blood. It has the same chemicals as clean blood, but without any blood cells. To see how the filtration works, well zoom in even further, to see the individual molecules in the blood and the dialysate. The membrane that separates the blood from the dialysate is semi-permeable. Small molecules like salts and toxins can move through the membrane easily, but the blood cells cannot. If any of the small molecules are at a higher concentration on one side of the membrane than on the other, they will cross the membrane. The levels of toxin will gradually become equal on both sides of the membrane, decreasing the amount of toxin in the blood, and increasing the amount of toxin in the dialysate. Then the dialysate is changed, and the process happens again. This is repeated until there are no more toxins, and then the blood is pumped back into the body. Hemodialysis, where dirty blood is pumped out, and clean blood pumped back in, is only one type of dialysis. Peritoneal dialysis is an alternative type of dialysis where blood never leaves the body. Instead, the abdominal cavity is used as a dialyzer. Hemodialysis, where dirty blood is pumped out, and clean blood pumped back in, is only one type of dialysis. Peritoneal dialysis is an alternative type of dialysis where blood never leaves the body. Instead, the abdominal cavity is used as a dialyzer. Dialysate is pumped into the abdominal cavity using a permanent catheter. The peritoneum is a semi-permeable membrane that lines the abdominal cavity. It is laced with tiny blood vessels. Toxins can easily pass through the peritoneum and enter the dialysate. The toxins continue to enter the dialysate until the concentration of toxins in the dialysate is equal to the concentration of toxins in the bloodstream. The dialysate fluid is then discarded, and new clean dialysate fluid is added. Again, the toxins move across the membrane until the concentration of toxin in the dialysate is equal to the concentration of toxin in the bloodstream. This process is repeated until the blood is clean. Hemodialysis and Peritoneal dialysis are both methods for filtering toxins out of the bloodstream without a kidney. Kidney transplantation is another method of replacing lost kidney function. One way to replace lost kidney function is to add a new kidney. Often the original kidneys are not removed, but a third one is added, either from a cadaver or a family member. This new kidney can take over the function of the original kidneys. Unfortunately, the transplant may not last. The body is adept at fighting off foreign invasion, and since the transplanted kidney is foreign tissue, it may be rejected by the immune system. To prevent this from happening, it is important to look for a very close match of kidney donor to patient. What does that mean? Every cell in the body is coated with specific "histocompatibility" or HLA proteins. The immune system recognizes these proteins, and uses them to identify "self." If a cell has the right set of HLA proteins, it belongs. If it does not, the immune system will remove it. There are so many different HLA proteins, and so many different combinations, that only identical twins are expected to match perfectly. However, the patient can take immune suppressant drugs. These drugs "blindfold" the immune system, making rejection of the transplanted kidney less likely. There are so many different HLA proteins, and so many different combinations, that only identical twins are expected to match perfectly. However, the patient can take immune suppressant drugs. These drugs "blindfold" the immune system, making rejection less likely. Immune suppressant drugs are strong enough that even a poorly matched kidney will probably last over a year. Unfortunately, other health-related problems may result due to a suppressed immune system. Kidney transplantation and dialysis are both ways of restoring lost kidney functions to PKD patients with kidney failure. Diagnosis Melissa explains how she found out she has PKD. Developing Symptoms Melissa describes the uncertainty of when and how her PKD symptoms will appear. Diet Awareness Melissa talks about her thoughts on her eating habits as a result of her PKD diagnosis. Dialysis Conflicts Melissa explains the different types of dialysis and how it complicates ones schedule. Transplants Melissa explains the risks of having an organ transplant. Changing Lifestyles Melissa describes how her mothers life has changed since her diagnosis. Finding Support Melissa describes different sources of support and how they have helped her. Alzheimer Disease
Renal Cystic Disease
The gross appearance of kidneys with recessive polycystic kidney disease (RPKD) is shown here. The bilaterally and symmetrically enlarged kidneys displace
http://www-medlib.med.utah.edu/WebPath/TUTORIAL/RENCYST/RCYST026.html
TMR - Polycystic Kidney Disease
This was my first exposure to polycystic kidney disease. polycystic kidney disease causes fluidfilled cysts to form in the kidneys, disrupting the
http://medicalreporter.health.org/tmr0795/polycyst0795.html

Extractions: By Joel R. Cooper Several years ago, I dated a woman whose father, a big computer company executive, had polycystic kidney disease. He received dialysis treatments at home, and was okay for a while, then developed complications and died. I remember seeing him at home on that machine which took blood from his body, then routed it into its mechanical innards and back into him after cleansing it somehow. Having never worked in a clinical environment before, seeing him lying there hooked up to a machine upon which he depended for life made me feel queasy and uncomfortable. Perhaps the experience reminded me of the fragility of life in general and my own mortality in particular. This was my first exposure to polycystic kidney disease. It had an impact. The woman, too, had the disease, which was genetically passed on to her from her father. A ballet instructor and choreographer, she's still very much alive today, but she has to be careful about her health and diet. And she knows her future is not necessarily very bright. She could die the same way her father did, if medical science can't produce a more palatable outcome for her. 600,000 Americans have the same disease she does, yet it's hardly a household term like AIDS. Polycystic kidney disease (PKD), sometimes called autosomal dominant polycystic kidney disease, is a life-threatening genetic disorder that eventually produces end-stage renal (kidney) disease in the majority of cases. Patients progressing to end-stage renal disease, must have either hemodialysis (a removal of the toxic substances in the blood by a machine that acts as an artificial kidney) or a kidney transplant to survive. According to the Polycystic Kidney Research Foundation, Kansas City, Missouri USA, an estimated 5 to 10 million people have the disease worldwide.
TMR - Interview
Treating polycystic kidney Disease What Does The Future Hold? Additionally, Dr. Grantham is Chairman of the polycystic kidney Research (PKR) Foundation
http://medicalreporter.health.org/tmr0795/interview0795.html

Extractions: Joel R. Cooper Dr. Grantham is Professor of Medicine at the University of Kansas Medical Center, Kansas City, Kansas, USA, and a member of the Nephrology and Hypertension Division of Internal Medicine. He has served in this position for 27 years. He also serves as Editor of The Journal of the American Society of Nephrology, headquartered at the University of Kansas Medical Center. Additionally, Dr. Grantham is Chairman of the Polycystic Kidney Research (PKR) Foundation, Kansas City, Missouri. His clinical and research training took place at the University of Kansas Medical Center, at The National Heart Institute, NIH (National Institutes of Health), Bethesda, Maryland, and at the Physiologic Laboratory, Cambridge, England. Dr. Grantham is widely regarded as one of the nation's leading authorities on polycystic kidney disease. I was able to reach Dr. Grantham thanks to Tanja Dunbar, Vice President of The PKR Foundation. I had a few definite questions I wanted to ask him on behalf of readers who either have polycystic kidney disease themselves, or who have friends or family members who do. My questions and Dr. Grantham's thoughtful responses follow. Joel R. Cooper, Editor
Polycystic Kidney Disease
polycystic kidney Disease (PKD1) in Cats. Introduction. polycystic kidney disease (PKD) is a well documented abnormality in domestic cats.
http://www.vgl.ucdavis.edu/service/cat/PKD.html

Extractions: Home Services Research Informatics ... Forensics Customer Service Phone: 530-752-2211 or email Services Polycystic kidney disease (PKD) is a well documented abnormality in domestic cats. Cystic kidneys can sporadically occur in any population of cats. PKD is not a new disease and has been reported in the literature for over 30 years. The heritable form of PKD1 may not have initially occurred in Persians as a new mutation, but perhaps in random bred cats. Unfortunately, PKD1 does not have a strong clinical presentation. The presentation of PKD1 is similar to one of the most common causes of death for any cat, renal failure. Thus, PKD1 has gone unnoticed for many years and has spread throughout the Persian breed. Any breed that has used Persians in their foundation or propagation should have concerns for PKD1. In Persians, the condition has been shown to be inherited as a single autosomal dominant gene. It is estimated over 37% of Persians have PKD1, a breed that accounts for nearly 80% of the cat fancy. Many lines and catteries have been able to greatly reduce this frequency by using ultrasound screening methods and improved breeding practices. Early onset, bilateral presentation (both kidneys), and multiple cysts are all traits of the heritable form of the disease. The kidney cysts for PKD1 present early, often before 12 months of age. Renal failure, however, usually occurs at a later age. Thus, PKD1 is considered a late onset renal disease. In the fancy cat breeds, PKD1 is inherited as an autosomal dominant condition. This implies that one copy of the gene is required to produce PKD1. Generally, 50% of PKD1 positive cats' offspring will inherit PKD1. A positive cat could potentially be homozygous for PKD1 and all offspring produced would have PKD1. It is suspected that cats that are homozygous for PKD1 are not abundant and the homozygote form could be lethal in utero or severely present at a very early age. Further research is required to prove the effects of the homozygote condition.
Polycystic Kidney Disease (PKD, Or PCKD)
Introduction polycystic kidney disease WrongDiagnosis.comIntroduction to polycystic kidney disease as a medical condition including symptoms, diagnosis, misdiagnosis, treatment, prevention, and prognosis.
http://renux.dmed.ed.ac.uk/EdREN/EdRenINFObits/PCKDLong.html

Extractions: from EdREN , the website of the Renal Unit of the Royal Infirmary of Edinburgh What happens in polycystic kidney disease? (PKD) Can anything else cause kidney cysts? What kidney trouble can PKD cause? What else can PKD do? ... Where can I get further information? Polycystic kidney disease (often shortened to PKD or PCKD ) is the commonest inherited cause of kidney failure. It may be inherited from either your mother or your father. Sometimes they will not know that they carry the disease. Not everyone with PKD gets trouble from their kidneys. It is quite common for healthy people to have one or two cysts, and occasionally people may have several. But when the kidney is filled with many cysts, PKD is the most likely diagnosis. There are some other rare diseases that very occasionally cause many kidney cysts. Infantile polycystic kidney disease is rare, causes liver damage as well as kidney trouble, and unfortunately often leads to affected children dying when they are young. It is not the same as the disease that occurs in adults. Up to contents What kidney trouble does PKD cause?
Introduction: Autosomal Dominant Polycystic Kidney Disease - WrongDiagnosis.com
Introduction to Autosomal dominant polycystic kidney disease as a medical condition including symptoms, diagnosis, misdiagnosis, treatment, prevention,
http://www.wrongdiagnosis.com/a/autosomal_dominant_polycystic_kidney_disease/int

Extractions: Autosomal dominant polycystic kidney disease: Autosomal dominant PKD is the most common, inherited form. Symptoms usually develop between the ages of 30 and 40, but they can begin earlier, even in childhood. About 90 percent of all PKD cases are autosomal dominant PKD. Researching symptoms of Autosomal dominant polycystic kidney disease: Further information about the symptoms of Autosomal dominant polycystic kidney disease is available including a list of symptoms of Autosomal dominant polycystic kidney disease , other diseases that might have similar symptoms in differential diagnosis of Autosomal dominant polycystic kidney disease , or alternatively return to research other symptoms in the
Polycystic Kidney Disease
polycystic kidney disease is an inherited kidney disorder that enlarges the kidneys and interferes with their function because of multiple cysts on the
http://www.healthcentral.com/ency/408/000502.html

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Clinical Trial: Evaluation Of Autosomal Recessive Polycystic Kidney Disease And
Autosomal recessive polycystic kidney disease longterm outcome of neonatal survivors. Pediatr Nephrol. 1997 Jun;11(3)302-6. Erratum in Pediatr Nephrol
http://www.clinicaltrials.gov/ct/show/NCT00068224

Extractions: Verified by National Institutes of Health Clinical Center (CC) June 20, 2005 Sponsored by: National Human Genome Research Institute (NHGRI) Information provided by: National Institutes of Health Clinical Center (CC) ClinicalTrials.gov Identifier: Purpose This study will evaluate patients with autosomal recessive polycystic kidney disease (ARPKD) and congenital hepatic fibrosis (CHF). People with ARPKD develop kidney cysts and eventually kidney failure, symptoms may include hypertension (high blood pressure), poor growth, and urinary infections. CHF is a specific type of liver disease associated with ARPKD. It involves fibrosis, or scarring, of the liver, which can lead to life-threatening complications, including internal bleeding of enlarged blood vessels called varices in the esophagus (food pipe). The goal of the study is to better understand the medical complications of ARPKD and CHF and identify characteristics that can help in the design of new treatments. Patients 6 months of age and older with ARPKD may be eligible for this 5- to 10-year study, excluding those who require frequent hospitalizations due to complications of end-stage renal disease or liver disease. Participants will undergo some or all of the following tests and procedures every 12 months during a 4- to 5-day hospital admission at the NIH Clinical Center:
Polycystic Kidney Disease
Genes and disease provides short descriptions of inherited disorders. It is hosted by the National Center for Biotechnology Information (NCBI),
http://www.ncbi.nlm.nih.gov/disease/PKD.html

Extractions: ADULT POLYCYSTIC kidney disease (APKD) is characterized by large cysts in one or both kidneys and a gradual loss of normal kidney tissue which can lead to chronic renal failure. The role of the kidneys in the body is to filter the blood, excreting the end-products of metabolism in the form of urine and regulating the concentrations of hydrogen, sodium, potassium, phosphate and other ions in the extracellular fluid. In 1994 the European Polycystic Kidney Disease Consortium isolated a gene from chromosome 16 that was disrupted in a family with APCD. The protein encoded by the PKD1 gene is an integral membrane protein involved in cell-cell interactions and cell-matrix interactions. The role of PKD1 in the normal cell may be linked to microtubule-mediated functions, such as the placement of Na(+), K(+)-ATPase ion pumps in the membrane. Programmed cell death, or apoptosis, may also be invoked in APKD. Further clarification of the pathogenesis of the disease await further research.
NEJM -- Polycystic Kidney Disease
Review Article from The New England Journal of Medicine polycystic kidney Disease.
http://content.nejm.org/cgi/content/extract/350/2/151

Extractions: Full Text PDF PDA Full Text Supplementary Material ... PubMed Citation Polycystic kidney diseases are a leading cause of end-stage renal failure and a common indication for dialysis or renal transplantation. Recent advances have led to insights into mechanisms underlying the cause and prognosis of these diseases and suggest new directions for treatment. Polycystic kidney disease may arise sporadically as a developmental abnormality or may be acquired in adult life, but most forms are hereditary. Among the acquired forms, simple cysts can develop in kidneys as a consequence of aging; dialysis, drugs, and hormones can cause multicystic disease ; and renal cysts are often secondary manifestations of genetic Full Text of this Article Autosomal Dominant Polycystic Kidney Disease Autosomal Recessive Polycystic Kidney Disease Familial Nephronophthisis Medullary Cystic Kidney Disease Cell Biology Proliferation and Apoptosis Secretion Polarity Signal Transduction Cilia Molecular Biology PKD Genes and Mutations Polycystic Kidney Disease Proteins Polycystin-1 Polycystin-2 Fibrocystin Nephrocystin Functions of Polycystins Developmental Regulation and Programming Prospects for Prognosis and Therapy
GeneReviews: Polycystic Kidney Disease, Autosomal Dominant
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To provide information, advice and support to those affected by polycystic kidney Disease PKD. Click here to learn more about ADPKD and ARPKD.
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Polycystic Kidney Disease
polycystic kidney Disease A. Characteristics See outline Chronic Renal Failure . Common hereditary disorder, ~0.2% of population
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Extractions: C. Pathogenesis Autosomal Dominant Disease caused by mutations in at least three genes PKD1 - codes for 4304 amino acid membrane protein called polycystin (chromosome 16) PKD2 - mapped to chromosome 4 Unidentified third locus Cyst formation in kidneys Abnormality in Na+/K+ ATPase Pump Cystic epithelium has pump in apical location Normal renal tubular epithelium has this pump on the basolateral surface Increased programmed cell death (apoptosis) in both dominant and recessive forms [ Mice with homozygous deletions in the proto-oncogene bcl-2 develop PKD [ Other mouse models (pcy and cpk) of the disease are now being studied
National Kidney Foundation: A To Z Health Guide
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