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Afferent arteriolopathy and glomerular collapse but not segmental sclerosis induce tubular atrophy in old spontaneously hypertensive rats

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dc.contributor.author Leh, Sabine
dc.contributor.author Hultström, Michael
dc.contributor.author Rosenberger, Christian
dc.contributor.author Iversen, Bjarne M.
dc.date.accessioned 2011-11-21T12:31:35Z
dc.date.available 2011-11-21T12:31:35Z
dc.date.issued 2011-06-10
dc.identifier.citation Virchows Archiv 459(1): 99-108 en
dc.identifier.issn 0945-6317
dc.identifier.uri http://dx.doi.org/10.1007/s00428-011-1100-3
dc.identifier.uri http://hdl.handle.net/1956/5208
dc.description.abstract In chronic renal disease, the temporal and spatial relationship between vascular, glomerular and tubular changes is still unclear. Hypertension, an important cause of chronic renal failure, leads to afferent arteriolopathy, segmental glomerulosclerosis and tubular atrophy in the juxtamedullary cortex. We investigated the pathological changes of hypertensive renal disease in aged spontaneously hypertensive rats using a large number of serial sections, where we traced and analyzed afferent arteriole, glomerulus and proximal tubule of single nephrons. Our major finding was that both afferent arteriolopathy and glomerular capillary collapse were linked to tubular atrophy. Only nephrons with glomerular collapse (n=13) showed tubules with reduced diameter indicating atrophy [21.66±2.56 μm vs. tubules in normotensive Wistar Kyoto rats (WKY) 38.56±0.56 μm, p<0.05], as well as afferent arteriolar wall hypertrophy (diameter 32.74±4.72 μm vs. afferent arterioles in WKY 19.24±0.98 μm, p<0.05). Nephrons with segmental sclerosis (n=10) did not show tubular atrophy and tubular diameters were unchanged (35.60±1.43 μm). Afferent arteriolar diameter negatively correlated with glomerular capillary volume fraction (r=−0.36) and proximal tubular diameter (r=−0.46) implying reduced glomerular and tubular flow. In line with this, chronically damaged tubules showed reduced staining for the ciliary protein inversin indicating changed ciliary signalling due to reduced urinary flow. This is the first morphological study on hypertensive renal disease making correlations between vascular, glomerular and tubular components of individual nephron units. Our data suggest that afferent arteriolopathy leads to glomerular collapse and reduced urinary flow with subsequent tubular atrophy. en
dc.language.iso eng en
dc.publisher Springer en
dc.relation.ispartof <a href="http://hdl.handle.net/1956/5961" target="blank">Progression of renal disease. Pathogenetic aspects and treatment options</a> en
dc.rights ©The Author(s) 2011 en
dc.rights.uri http://www.springer.com/open+access/open+choice?SGWID=0-40359-0-0-0 en
dc.subject Glomerular collapse en
dc.subject Tubular atrophy en
dc.title Afferent arteriolopathy and glomerular collapse but not segmental sclerosis induce tubular atrophy in old spontaneously hypertensive rats en
dc.type Peer reviewed en
dc.type Journal article en
dc.subject.nsi VDP::Medical disciplines: 700::Clinical medical disciplines: 750::Nephrology, urology: 772 en
dc.type.version publishedVersion en


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