id,collection,dc.contributor.author,dc.contributor.firstReferee,dc.contributor.furtherReferee,dc.contributor.gender,dc.date.accepted,dc.date.accessioned,dc.date.available,dc.date.issued,dc.description.abstract[de],dc.description.abstract[en],dc.format.extent,dc.identifier.uri,dc.identifier.urn,dc.language,dc.rights.uri,dc.subject.ddc,dc.title,dc.title.translated[en],dc.type,dcterms.accessRights.dnb,dcterms.accessRights.openaire,dcterms.format[de],refubium.affiliation[de],refubium.mycore.derivateId,refubium.mycore.fudocsId "2e7315b1-86b8-45c7-b72e-2ab812a7ab48","fub188/13","Gadau, Juliane","Prof. Dr. S. Bachmann","Prof. Dr. G. Burckhardt||Prof. Dr. M. Bader","n","2009-01-30","2018-06-07T22:35:19Z","2008-12-04T08:05:11.539Z","2009","Das nephritische Syndrom ist ein durch Hämaturie, Proteinurie und Ödeme gekennzeichneter Symptomkomplex, meist als Folge einer akuten Glomerulonephritis (GN). Intrarenale epitheliale Veränderungen, die zu Antinatriurese führen können, wurden als Ursache der Volumenretention im nephritischen Tiermodell Anti-Thy1-GN untersucht. Ratten mit Anti-Thy1-GN entwickelten Proteinurie und Lipidurie. Natriurese, glomeruläre Filtrationsrate und Renin-Angiotensin-Aldosteron-System (RAAS)-Parameter waren reduziert. Die Expressionsabnahmen proximal lokalisierter Transporter waren mit zellulärer Protein- und Cholesterolüberladung sowie zytoskelettären Veränderungen verbunden und könnten durch diese mitbedingt sein. In der Henle’schen Schleife blieben die Veränderungen weitgehend unspezifisch. Im spätdistalen Tubulus und Sammerohr waren die Expression des epithelialen Natriumkanals (ENaC) vermehrt. Unter nephritischen Bedingungen ist die Aktivierung von ENaC-Untereinheiten durch eine enzymatische Spaltung durch glomerulär gefilterte Proteasen denkbar. Der ENaC-vermittelte Natriumeintritt scheint der bestimmende sowie limitierende Faktor der Natriumrückresorption am Sammelrohr zu sein.","The nephritic syndrome is a clinically symptom complex which often develops following acute glomerulonephritis (GN). It is characterized by hematuria, proteinuria, hypertension, and edema formation. The origins of volume retention in GN are controversially discussed. The hypothesis was followed that disturbed salt- and water homeostasis has its origin in kidney-based epithelial changes causing antinatriuresis. Rats with GN induced by anti-Thy1 antibody were studied. Anti-Thy1-GN rats had pronounced proteinuria and lipiduria associated with reduced glomerular filtration rate, low renin- angiotensin-aldosterone system (RAAS) parameters, no change in vasopressin, and sodium retention. Exploring the underlying mechanisms a reduced abundance of proximal tubular brush border membrane expression of the major salt- and water transport proteins along with cellular protein and cholesterol overload and cytoskeletal changes were observed. Alterations in the loop of Henle's segments were moderate. Collecting ducts were characterized by enhanced abundance and increases in subunit cleavage of the epithelial sodium channel (ENaC). Irrespective of the proximal tubular changes, likely to be caused by the protein and lipid overload, ENaC-mediated sodium entry may be the rate- limiting step in collecting duct-based sodium retention. Mechanisms of ENaC activation under nephritic proteinuria which involves its proteolytic cleavage by means of filtered plasma proteases can propose.","83","https://refubium.fu-berlin.de/handle/fub188/9422||http://dx.doi.org/10.17169/refubium-13621","urn:nbn:de:kobv:188-fudissthesis000000006427-8","ger","http://www.fu-berlin.de/sites/refubium/rechtliches/Nutzungsbedingungen","600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit","Tubulo-epitheliale Einflüsse auf die Volumenretention bei akuter Anti- Thy1-Glomerulonephritis","Tubular involvement in volume retention during acute experimental anti-Thy1 glomerulonephritis","Dissertation","free","open access","Text","Charité - Universitätsmedizin Berlin","FUDISS_derivate_000000011285","FUDISS_thesis_000000006427"