Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9169
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dc.contributor.authorJandeleit-Dahm, Ken
dc.contributor.authorCao, Zeminen
dc.contributor.authorCox, Allison Jen
dc.contributor.authorKelly, D Jen
dc.contributor.authorGilbert, Richard Een
dc.contributor.authorCooper, Mark Een
dc.date.accessioned2015-05-15T22:09:23Z
dc.date.available2015-05-15T22:09:23Z
dc.date.issued1999-07-01en
dc.identifier.citationKidney International. Supplement; 71(): S31-6en
dc.identifier.govdoc10412733en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/9169en
dc.description.abstractIt has been suggested that lipids promote renal injury and that 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors confer renoprotection in certain renal diseases, including diabetic nephropathy.Sprague-Dawley rats were randomized to sham, subtotal nephrectomy (STNx) or STNx + atorvastatin groups. After 12 weeks, proteinuria, renal function, glomerular injury, renal transforming growth factor-beta (TGF-beta) gene expression and macrophage (ED1-positive cells) accumulation were assessed. In addition, the effects of HMG CoA reductase in human diabetic nephropathy were reviewed.Atorvastatin therapy was associated with a modest reduction in proteinuria and glomerulosclerosis without influencing lipid levels or renal function in STNx rats. These effects were associated with decreased renal TGF-beta 1 gene expression and less glomerular and tubulointerstitial macrophage accumulation. The renoprotective effects of HMG CoA reductase inhibitors in both insulin- and non-insulin-dependent diabetic subjects with either incipient or overt nephropathy appear to be highly variable.HMG CoA reductase inhibition appears to confer renoprotection via effects on prosclerotic cytokines such as TGF-beta and macrophage accumulation, independent of their lipid-lowering properties. The role of lipid-lowering agents in early or overt diabetic nephropathy remains to be fully ascertained.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherAnticholesteremic Agents.therapeutic useen
dc.subject.otherClinical Trials as Topicen
dc.subject.otherDiabetic Nephropathies.drug therapyen
dc.subject.otherDisease Progressionen
dc.subject.otherGene Expression.drug effectsen
dc.subject.otherHeptanoic Acids.therapeutic useen
dc.subject.otherHumansen
dc.subject.otherHydroxymethylglutaryl-CoA Reductase Inhibitors.therapeutic useen
dc.subject.otherHyperlipidemias.physiopathologyen
dc.subject.otherIn Situ Hybridizationen
dc.subject.otherKidney Diseases.drug therapy.pathology.physiopathologyen
dc.subject.otherKidney Glomerulus.drug effects.metabolism.pathologyen
dc.subject.otherLovastatin.therapeutic useen
dc.subject.otherMaleen
dc.subject.otherNephrectomyen
dc.subject.otherPravastatin.therapeutic useen
dc.subject.otherPyrroles.therapeutic useen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherSimvastatin.therapeutic useen
dc.subject.otherTransforming Growth Factor beta.geneticsen
dc.titleRole of hyperlipidemia in progressive renal disease: focus on diabetic nephropathy.en
dc.typeJournal Articleen
dc.identifier.journaltitleKidney International. Supplementen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin, Victoria, Australiaen
dc.description.pagesS31-6en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/10412733en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
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