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Antioxidants and iron chelators have also been shown to retard functional and
morphologic changes observed in progressive kidney disease
<<snip>>
Kidney Int Suppl. 2004 Oct(91):S50-5. Links
Oxidants and iron in chronic kidney disease.
Shah SV.
Division of Nephrology, Department of Medicine, university of Arkansas for
Medical Sciences, Little Rock, Arkansas.
Oxidants and iron in chronic kidney disease. Oxidants derived either from
leukocytes in proliferative glomerular nephritis or from resident glomerular
cells in nonproliferative glomerulonephritis have been shown to have several
biologic effects relevant to chronic kidney disease. These include: the ability
of oxidants to damage glomerular basement membrane (GBM) and to directly induce
proteinuria; effects that would lead to a fall in the glomerular filtration
rate; and effects that would account for the morphologic changes observed in
chronic kidney disease. In experimental models the role of oxidants has been
demonstrated in both proliferative glomerulonephritis (e.g., anti-GBM antibody
disease) as well as experimental models of minimal change disease and
membranous nephropathy. Oxidants have also been shown to be an important
mediator of the various pathways that have been implicated in diabetic
nephropathy. Antioxidants and iron chelators have also been shown to retard
functional and morphologic changes observed in progressive kidney disease.
Taken together, these experimental studies suggest an important role of
oxidants in chronic kidney disease.
PMID: 15461704 [PubMed - in process]
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