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Polycystic Kidney:     more books (43)

Medifocus Guidebook on: Polycystic Kidney Disease by Medifocus.com Inc., 2010-07-21 The Official Patient's Sourcebook on Polycystic Kidney Disease Polycystic Kidney Disease (Oxford Clinical Nephrology Series) Autosomal Dominant Polycystic Kidney Desease: Seminar on Autosomal Dominant Polycystic Kidney Disease, Vimercate, June 18, 1994 (Contributions to Nephrology) by Seminar on Autosomal Dominant Polycystic Kidney Disease, A. Sessa, 1995-12 Polycystic Kidney Disease (Contributions to Nephrology) by M. H. Breuning, M. Devoto, 1992-07 ADPKD patients manual: Understanding and living with autosomal dominant polycystic kidney disease by Irene T Duley, 1995 Problems in Diagnosis and Management of Polycystic Kidney Disease: Proceedings of the First International Workshop on Polycystic Kidney Disease The Cystic Kidney (Developments in Nephrology) Conquering Kidney Disease - Identifying Potential Problems by Merle Fields, 2010-05-31 Health tips for living with polycystic kidney disease by Arlene B Chapman, 2001 Polycystic kidney disease: An entry from Thomson Gale's <i>Gale Encyclopedia of Genetic Disorders, 2nd ed.</i> by Paul Johnson, 2005 ADVANCES IN THE PATHOGENESIS OF POLYCYSTIC KIDNEY DISEASE by F.; Dobbie, J.W. Carone, 1990 PKD patient's manual: Understanding & living with autosomal dominant polycystic kidney disease by Irene Duley, 1989 Polycystic Kidney Disease Medical Guide by Qontro Medical Guides, 2008-07-09

lists with details

101. Polycystic Kidney Disease
     a CHORUS notecard document about polycystic kidney disease.  
     http://chorus.rad.mcw.edu/doc/00328.html

102. Pkd Polycystic Kidney Disease
     Feline PKDAutosomal dominant polycystic kidney genetic non sex, polycystic kidney disease (PKD) in Persian cats has been increasingly reported and  
     http://www.thensome.com/pdk.htm
     
     Extractions: Feline PKD-Autosomal dominant polycystic kidney genetic non sex, non color linked cat disease can be diagnosed as early as seven weeks old with abdominal ultrasound. The cysts will appear as black and round. Persians and Persian crossbred cats are most often affected by this disease which can result in renal failure. Not all cats will show signs of the disease which are classic signs of renal failure:Weight loss, poor appetite, increased thirst and urination, lack of energy, and vomiting The iohexol clearance test is a sensitive blood test that may detect kidney problems before the symptoms emerge usually after 2/3s of damage. Dietary citrate treatment and flaxseed may help..research on cats is needed(please check out the research abstracts below) Breeders are growing more knowledgeable and responsible. < P < or = .1). No significant differences were found between the groups in serum aldosterone and plasma ANP concentrations. None of the cats had echocardiographic evidence of cardiac hypertrophy. In conclusion, cats with PKD had a minor increase in mean arterial pressure compared to control cats, and half of the cats had a high ARR.

103. Polycystic Kidney Disease - DaVita
     polycystic kidney disease (PKD) happens when fluidfilled cysts form in the kidneys. It is a chronic kidney disease, which can lead to end stage renal  
     http://www.davita.com/articles/ckd/index.shtml?id=511

104. POLYCYSTIC KIDNEY DISEASE
     polycystic kidney DISEASE. View image. The axial CT scan done with intravenous contrast demonstrates the presence of bilaterally enlarged kidneys  
     http://www.netmedicine.com/xray/ctscan/cta22.htm
     
     Extractions: POLYCYSTIC KIDNEY DISEASE View image The axial CT scan done with intravenous contrast demonstrates the presence of bilaterally enlarged kidneys (asterisks) a solitary cyst of the polycystic kidneys is marked with the arrow heads. The left kidney demonstrates the presence of a calcified cyst wall as the result of a previous infection or hemorrhage. The presence of a fluid/fluid level within a cyst may indicate either hemorrhage or infection. NetMedicine Home Page CT Scan Library Downloading and using one of these free programs as a helper application will significantly improve JPEG image quality

105. HALT PKD Home
     The polycystic kidney Disease Treatment Network (PKDTN) has established the HALT PKD Key Resources for Information on polycystic kidney Disease  
     http://www.pkd.wustl.edu/pkdtn/
     
     Extractions: Polycystic Kidney Disease Treatment Network HALT PKD HALT PKD Clinical Research The Polycystic Kidney Disease Treatment Network (PKD-TN) has established the HALT PKD HALT PKD clinical trials. The Division of Biostatistics at Washington University in St. Louis serves as the Data Coordinating Center (DCC), under the guidance of Professor J. Philip Miller. The DCC is responsible for developing a Web-based data entry system, managing all study data, tracking patient recruitment and adverse events, and overseeing data collection and reporting. Please note that final determination of eligibility to participate in any clinical trial requires that the principal investigator or his/her designate make a very subject-specific, case-by-case assessment based on defined inclusion/exclusion criteria. Key Resources for Information on Polycystic Kidney Disease PKD Foundation The PKD Foundation is the only organization, worldwide, devoted to determining the cause, improving clinical treatment and discovering a cure for Polycystic Kidney Disease (PKD).

106. Autosomal Dominant Polycystic Kidney Disease Knowledgebase
     Background Autosomal dominant polycystic kidney disease (ADPKD) affects approximately one in 800 people worldwide resulting in bilateral renal tubular cyst  
     http://www.cimr.cam.ac.uk/medgen/pkd/default.htm
     
     Extractions: Background Autosomal dominant polycystic kidney disease (ADPKD) affects approximately one in 800 people worldwide resulting in bilateral renal tubular cyst formation and eventually renal failure. Two proteins, polycystin 1 (the PKD1 gene product) and polycystin 2 (the PKD2 gene product) are central to this condition with PKD1 mutations accounting for 85% of all ADPKD cases and PKD2 responsible for the majority of the rest. Polycystin-1 is an eleven membrane spanning protein of 4303 amino acids of as yet unknown function. Polycystin-2 is a 968 amino acid protein having 6 membrane spanning domains and again has no ascribed function although may be involved in ion channel formation. Research Aims: The Renal Genetics Group's principle focus is the molecular and pathophysiology of ADPKD. Mutation analysis, structural studies and the development of in vitro and in vivo models are currently being developed. Other work concentrates on other forms of inherited renal disease and the use of comparative genomics to identify functional domains of disease genes. ADPKD and Renal Web Links

107. Rural Nurse Organization Clinic Digital Library
     Autosomal Dominant polycystic kidney Disease Access document Recessive polycystic kidney Disease, Gross Access document; Recessive polycystic kidney  
     http://ruralnurseorganization-dl.slis.ua.edu/clinical/nephrology/renaltubulardis
     
     Extractions: Clinical Resources by Topic: Nephrology Polycystic Kidney Diseases Clinical Resources Pediatrics Atlases Radiology Pathology ... Miscellaneous Resources See also: Medicine, Ob/Gyn, Psychiatry, and Surgery (eMedicine): Table of contents Pediatrics Resources See also General Pediatrics Resources Atlases Radiology Resources See also General Radiology Resources CHORUS-Collaborative Hypertext of Radiology: Homepage Pathology Resources Internet Pathology Lab for Medical Education (FSU Coll of Med): Table of contents Mini-Tutorials: List of documents Recessive Polycystic Kidney Disease (RPKD):

108. ARPKD/PKHD1 Mutation Database
     Autosomal Recessive polycystic kidney Disease (ARPKD/PKHD1) PKHD1 (polycystic kidney and Hepatic Disease 1) is a large gene spanning 470 kb of genomic  
     http://www.humgen.rwth-aachen.de/
     
     Extractions: Group Aachen It has been crucial to catalogue all changes detected in in a locus specific database. Investigators are invited to submit their novel data to this database. These data should be meaningful for clinical practice as well as of relevance for the reader interested in molecular aspects of polycystic kidney disease (PKD). There are also some links and information for ARPKD patients and their parents. Amendments and suggestions are welcomed. For more detailed questions please contact us (cbergmann@ukaachen.de) Our research group uses a multidisciplinary approach to understand the genetic and cellular basis of polycystic kidney disease (PKD). The PKDs are a group of inherited disorders that result in renal cyst development often leading to end-stage renal disease. The overall aim of these studies is to understand the normal function of the PKD proteins and define the pathobiology associated with mutations so that rational therapies can be developed for these disorders in future years. There are two major forms of PKD: Autosomal Dominant (ADPKD) and Autosomal Recessive (ARPKD). ADPKD is one of the most common monogenic disorders with a frequency of 1/500-1000. About 5% of all patients requiring renal replacement therapy (kidney transplant or dialysis) are affected by ADPKD. In most cases of ADPKD (~80%), patients carry a mutation in the PKD1 gene on chromosome 16p13, whereas 10-15% harbour a mutation in the PKD2 gene on chromosome 4q21. While ADPKD is usually a disease of adults, about 1-2% of patients display an early manifesting clinical course and may die perinatally.

109. GENES INVOLVED IN POLYCYSTIC KIDNEY DISEASE
     Item Image, GENES INVOLVED IN polycystic kidney DISEASE. polycystic kidney disease is an autosomal dominant disorder. Worldwide, this disease accounts for  
     http://www.bioscience.org/news/scientis/urine.htm
     
     Extractions: SCIENCE NEWS DIGEST FOR PHYSICIANS AND SCIENTISTS GENES INVOLVED IN POLYCYSTIC KIDNEY DISEASE Polycystic kidney disease is an autosomal dominant disorder. Worldwide, this disease accounts for 8-10% of end stage kidney disease and results in chronic renal failure in about 45% of the affected individuals by the age of 60. The patients with the disease develop cysts in both kidneys that gradually enlarge over the lifetime of the individual and ultimately lead to chronic renal failure and hypertension. At least two loci are known to exist for this disease. One locus was designated PKD4. By analysis of a genomic cosmid clone and cDNA, Lisowsky et al identified a new human gene on chromosome 16 (16p13.3) in the locus for polycystic kidney disease (PKD1). The gene contains at least one intron and is actively transcribed in tissues from kidney and brain. The predicted protein was homologous (42%) to the yeast scERV1 protein which is essential for oxidative phosphorylation, the maintenance of mitochondrial genomes, and the cell-division cycle. A second locus is present on chromosome 4q (4q21-23). In the May 31, 1996 issue of Science, Mochizuki et al describe identification of a second gene by positional cloning, whose nonsense mutation leads to this disease. The predicted protein consists of 968 amino acids and contains six transmembrane spans with both amino- and carboxyl termini residing in the cytoplasm. This protein shows amino acid similarity to the previously described PKD1 as well as the C elegans homolog of PKD1. The protein contains one potential calcium binding site and it is interesting that there is amino acid identity between this protein and the members of the family of voltage-activated calcium and sodium channels.

110. American Family Physician: Polycystic Kidney Disease
     Full text of the article, polycystic kidney disease from American Family Physician, a publication in the field of Health Fitness, is provided free of  
     http://www.findarticles.com/p/articles/mi_m3225/is_1_71/ai_n8702979
     
     Extractions: Save a personal copy of this article and quickly find it again with Furl.net. It's free! Save it. What do the kidneys do? Kidneys remove waste products from your blood. They do this by filtering the blood and making urine. The urine carries waste products out of your body. What is polycystic kidney disease?

111. FIRSTConsult - Sdfdsf
     FIRSTConsult, polycystic kidney disease (Patient Education File). Published for medical students and primary healthcare providers by Elsevier.  
     http://www.firstconsult.com/?action=view_article&id=1037485&type=103&bref=1

112. Virtual Children's Hospital: Paediapaedia: Infantile / Juvenile Polycystic Kidne
     Infantile / Juvenile polycystic kidney Disease (Autosomal Recessive polycystic kidney Disease). Michael P. D Alessandro, MD Peer Review Status Internally  
     http://www.vh.org/pediatric/provider/radiology/PAP/GUDiseases/IPCKD.html
     
     Extractions: A spectrum of disease involving the kidneys and liver. The infantile form presents earlier and involves primarily the kidneys, while the juvenile form presents later and involves primarily the liver. The infantile form can expire in the newborn period from pulmonary hypoplasia associated with fetal anuria or present later in infancy with renal failure. The juvenile form presents at 5-10 years old with hepatosplenomegaly and hematemesis due to varices. Etiology/Pathophysiology: Due to dilated renal collecting tubules located throughout the kidneys. Also have hepatic fibrosis, bile duct hyperplasia, and variable parenchymal cysts. The classification as infantile or juvenile forms depends on the amount of renal disease present. In the infantile form there is severe renal involvement with incidental hepatic disease with enlarged kidneys filled with microcysts which give a spongelike cross sectional appearance to the renal cortex and medulla. In the juvenile form there is congenital hepatic fibrosis with renal tubule ectasia. This dominant hepatic fibrosis with minimal renal involvement leads to portal hypertension and varices. The kidneys are less cystic and have cysts and renal tubular ectasia primarily in the medulla.

113. Researchers Identify Novel Treatment For Polycystic Kidney Disease In Animals
     The drug OPC31260 stops the development of cysts and prevents kidney function loss in rats and mice, according to a Mayo Clinic and Indiana University  
     http://www.eurekalert.org/pub_releases/2003-09/mc-rin092903.php
     
     Extractions: Mayo Clinic ROCHESTER, Minn. The drug OPC31260 stops the development of cysts and prevents kidney function loss in rats and mice, according to a Mayo Clinic and Indiana University School of Medicine study published in the October 2003 issue of Nature Medicine. Inherited diseases that cause the kidneys to develop fluid-filled cavities (cysts) are major causes of kidney failure in children and in adults. The most common and important diseases in this category are autosomal dominant polycystic kidney disease (ADPKD) in adults, and autosomal recessive polycystic kidney disease (ARPKD) and nephronophthisis in children. Currently, there are no effective treatments for these disorders. Previous studies conducted at the University of Kansas and other polycystic kidney disease research centers showed that a chemical compound known as cyclic AMP is largely responsible for the cell proliferation and fluid secretion that are central to the development of kidney cysts. The drug studied by Mayo Clinic and Indiana University researchers inhibits the production of cyclic AMP by blocking a specific receptor found almost exclusively on the cells from which the cysts develop. In healthy kidneys, cyclic AMP stimulates the reabsorption of water by these cells, which normally do not proliferate and form cysts.

114. Polycystic Kidney Disease, Autosomal Recessive
     polycystic kidney and hepatic disease 1. polycystic kidney disease, infantile, Autosomal Recessive polycystic kidney Disease RadiologicPathologic  
     http://www.gfmer.ch/genetic_diseases_v2/gendis_detail_list.php?cat3=661

115. Renal Pathology
     This kidney in a patient with DPKD weighed 3 kilograms! This disease is inherited with an autosomal dominant pattern, so the recurrence risk in the family  
     http://www-medlib.med.utah.edu/WebPath/RENAHTML/RENAL049.html
     
     Extractions: This kidney in a patient with DPKD weighed 3 kilograms! This disease is inherited with an autosomal dominant pattern, so the recurrence risk in the family is 50%. The cysts are not usually present at birth, but develop slowly over time, so the onset of renal failure occurs in middle age to later adult life.

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