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http://www.tkuhn.ch/bel2nanopub/RAbLOI3R2gNEQALEXKW6br1-B69tphFb1cuGqXcHeolWQ#_1
http://purl.obolibrary.org/obo/BFO_0000066
http://purl.obolibrary.org/obo/UBERON_0002113
http://www.tkuhn.ch/bel2nanopub/RAbLOI3R2gNEQALEXKW6br1-B69tphFb1cuGqXcHeolWQ#_1
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http://www.w3.org/1999/02/22-rdf-syntax-ns#object
http://resource.belframework.org/belframework/20131211/namespace/selventa-legacy-diseases/nephropathy
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http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
http://purl.bioontology.org/ontology/MSH/D006973
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http://www.w3.org/2000/01/rdf-schema#label
path(MESHD:Hypertension) -> path(SDIS:nephropathy)
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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C. A. O'Callaghan, Barry M. Brenner
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http://purl.org/dc/elements/1.1/title
C. A. O'Callaghan, Barry M. Brenner
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Other
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The primary insult is damage to the renal vessels from the raised pressure. In the interlobular artery walls, muscle is replaced by sclerotic tissue. The afferent arteriole walls undergo hyalinization - the subintimal deposition of lipids and glycoproteins exuded from plasma. Damage to these resistance vessels exposes the glomerular capillary endothelium to hypertension. This reduces glomerular blood flow and filtration, and promotes proteinuria. Inflammatory proteins are exuded from the plasma and ultimately there is glomerular sclerosis or ischemic atrophy.
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Selventa
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http://www.w3.org/ns/prov#wasDerivedFrom
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2014-07-03T14:31:29.307+02:00
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