title: Antiproteinuric effect of RAS blockade: new mechanisms.
abstract: Experimental and clinical studies have shown that blockade of the renin-angiotensin system (RAS) is effective in reducing proteinuria in conditions such as diabetes by reducing systemic and intraglomerular hydrostatic pressure. However, increasing evidence suggests that nonhemodynamic effects, such as preservation of the podocyte slit diaphragm structure and function, may also mediate the antiproteinuric effects of RAS blockade. In this review, we analyze in detail the evidence for known and novel mechanisms considered to play important roles in mediating the antiproteinuric effect of RAS blockers, with a particular focus on diabetic nephropathy.
authors.affiliation: Vascular Division, The Baker Heart Research Institute, Commercial Road, Melbourne 3004, Victoria, Australia.
authors.forename: Markus
authors.initials: M
authors.lastname: Lassila
authors.forename: Mark E
authors.initials: ME
authors.lastname: Cooper
authors.forename: Karin
authors.initials: K
authors.lastname: Jandeleit-Dahm
mesh_terms: D000419:Albuminuria / Q000209:etiology / Q000517:prevention & control; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage*; D000818:Animals; D001707:Biopsy, Needle; D002986:Clinical Trials as Topic; D003921:Diabetes Mellitus, Experimental; D003928:Diabetic Nephropathies / Q000188:drug therapy* / Q000473:pathology*; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects; D006801:Humans; D007150:Immunohistochemistry; D051379:Mice; D008812:Mice, Hairless; D051381:Rats; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology; D012680:Sensitivity and Specificity; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D042461:Vascular Endothelial Growth Factor A