Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13626
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dc.contributor.authorJohnston, Colin Ien
dc.contributor.authorRisvanis, Johnen
dc.contributor.authorNaitoh, Men
dc.contributor.authorTikkanen, Ilkkaen
dc.date.accessioned2015-05-16T03:30:59Z
dc.date.available2015-05-16T03:30:59Z
dc.date.issued1998-09-01en
dc.identifier.citationJournal of Hypertension. Supplement; 16(4): S3-7en
dc.identifier.govdoc9817185en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/13626en
dc.description.abstractHypertension, a known independent risk factor for end-stage renal failure, damages the kidney in multiple ways. It produces hemodynamic and mechanical stress, which may lead to glomerular endothelial dysfunction. Both of these mechanisms may lead to increased glomerular leakiness, hence proteinuria, which may damage the kidney further. Hypertension may also stimulate the production of vasoactive substances that, in turn, activate the production of cytokines and growth factors, leading to the production of extracellular matrix proteins. Thus, the progression of renal failure is related to both systemic and glomerular hemodynamic changes and to the activation of vasoactive hormones, growth factors and cytokines.To protect the kidney, we need to control or prevent the occurrence of these factors. Therapy with effective antihypertensive agents, such as angiotensin-converting enzyme inhibitors, has been shown to slow the progression of end-stage renal disease.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherAntihypertensive Agents.therapeutic useen
dc.subject.otherDisease Progressionen
dc.subject.otherHemodynamics.physiologyen
dc.subject.otherHumansen
dc.subject.otherKidney.physiopathologyen
dc.subject.otherKidney Diseases.physiopathology.prevention & controlen
dc.subject.otherRenin-Angiotensin System.physiologyen
dc.titleMechanism of progression of renal disease: current hemodynamic concepts.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Hypertension. Supplementen
dc.identifier.affiliationThe University of Melbourne, Department of Medicine, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australiaen
dc.description.pagesS3-7en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/9817185en
dc.type.austinJournal Articleen
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
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