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Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13635
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dc.contributor.authorCooper, Mark Een
dc.contributor.authorGilbert, Richard Een
dc.contributor.authorEpstein, Men
dc.date.accessioned2015-05-16T03:31:18Z
dc.date.available2015-05-16T03:31:18Z
dc.date.issued1998-12-01en
dc.identifier.citationMetabolism: Clinical and Experimental; 47(12 Suppl 1): 3-6en
dc.identifier.govdoc9867062en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/13635en
dc.description.abstractDiabetic nephropathy (DN) is now the commonest cause of end-stage renal failure in the Western world. Recent studies examining the pathogenesis of diabetic complications have focused on the complex interaction between genetic and hemodynamic mechanisms in addition to metabolic factors such as advanced glycation, protein kinase C (PKC) activation, and polyol production. The importance of the various components, particularly with regard to the progression of DN, is currently being explored with the assistance of targeted drug intervention studies.en
dc.language.isoenen
dc.subject.otherDiabetic Nephropathies.genetics.metabolism.physiopathology.therapyen
dc.subject.otherGlycosylation End Products, Advanced.metabolismen
dc.subject.otherHemodynamics.physiologyen
dc.subject.otherHumansen
dc.subject.otherPolymers.metabolismen
dc.titlePathophysiology of diabetic nephropathy.en
dc.typeJournal Articleen
dc.identifier.journaltitleMetabolism: clinical and experimentalen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin & Repatriation Medical Centre, Heidelberg, Victoria, Australiaen
dc.description.pages3-6en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/9867062en
dc.type.austinJournal Articleen
item.fulltextNo Fulltext-
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
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