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pubmed-article:15119204rdf:typepubmed:Citationlld:pubmed
pubmed-article:15119204lifeskim:mentionsumls-concept:C1328818lld:lifeskim
pubmed-article:15119204lifeskim:mentionsumls-concept:C0033687lld:lifeskim
pubmed-article:15119204lifeskim:mentionsumls-concept:C0277785lld:lifeskim
pubmed-article:15119204pubmed:issue15lld:pubmed
pubmed-article:15119204pubmed:dateCreated2004-5-3lld:pubmed
pubmed-article:15119204pubmed:abstractTextPodocytes play a central role in the pathogenesis of several glomerular diseases. In recent years, this has been revealed by molecular analysis of a number of rare hereditary renal diseases. Podocytes contain three domains: the domain bound to the glomerular basement membrane (GBM), the domain of the slit diaphragms and the apical domain. The slit diaphragms are situated basolaterally between the pedicles and form together with the GBM a mechanism for the selective filtration of blood to primary urine. The apical cell membrane forms a negatively charged layer which prevents adhesion to the adjacent cell membranes, thus keeping the slit diaphragms and urinary space open. Many podocyte diseases are characterised by foot process effacement, which causes the loss of slit diaphragms, and could lead to podocyte loss. Specific abnormalities have been discovered in the three domains of the podocyte to which a number of glomerular diseases can be attributed.lld:pubmed
pubmed-article:15119204pubmed:languagedutlld:pubmed
pubmed-article:15119204pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15119204pubmed:citationSubsetIMlld:pubmed
pubmed-article:15119204pubmed:statusMEDLINElld:pubmed
pubmed-article:15119204pubmed:monthAprlld:pubmed
pubmed-article:15119204pubmed:issn0028-2162lld:pubmed
pubmed-article:15119204pubmed:authorpubmed-author:BerdenJ HJHlld:pubmed
pubmed-article:15119204pubmed:authorpubmed-author:van der...lld:pubmed
pubmed-article:15119204pubmed:authorpubmed-author:VogtländerN...lld:pubmed
pubmed-article:15119204pubmed:authorpubmed-author:RietjensS JSJlld:pubmed
pubmed-article:15119204pubmed:issnTypePrintlld:pubmed
pubmed-article:15119204pubmed:day10lld:pubmed
pubmed-article:15119204pubmed:volume148lld:pubmed
pubmed-article:15119204pubmed:ownerNLMlld:pubmed
pubmed-article:15119204pubmed:authorsCompleteYlld:pubmed
pubmed-article:15119204pubmed:pagination712-8lld:pubmed
pubmed-article:15119204pubmed:dateRevised2006-11-15lld:pubmed
pubmed-article:15119204pubmed:meshHeadingpubmed-meshheading:15119204...lld:pubmed
pubmed-article:15119204pubmed:meshHeadingpubmed-meshheading:15119204...lld:pubmed
pubmed-article:15119204pubmed:meshHeadingpubmed-meshheading:15119204...lld:pubmed
pubmed-article:15119204pubmed:year2004lld:pubmed
pubmed-article:15119204pubmed:articleTitle[Podocyte dysfunction and proteinuria].lld:pubmed
pubmed-article:15119204pubmed:affiliationUniversitair Medisch Centrum St Radboud, afd. Nierziekten, Postbus 9101, 6500 HB Nijmegen.lld:pubmed
pubmed-article:15119204pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15119204pubmed:publicationTypeEnglish Abstractlld:pubmed
pubmed-article:15119204pubmed:publicationTypeReviewlld:pubmed
pubmed-article:15119204pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed