That reactive oxygen species are involved in progressive renal injury is su
pported by several lines of evidence: increased generation of oxidants occu
rs in chronic renal injury; various antioxidant strategies exert beneficial
effects in models of chronic renal injury; and, oxidative stress can induc
e changes in the otherwise unmanipulated kidney that resemble those seen in
chronic renal disease. Oxidants may contribute to progressive renal diseas
e by virtue of their renal haemodynamic actions, by impairing glomerular pe
rmselective properties, by inducing inordinate or aberrant growth responses
, by inducing loss of cellular phenotype and apoptosis, and finally, by pro
moting acute and chronic inflammatory responses. Certain adhesion molecules
and proinflammatory mediators, and the transcription factor NF kappa B, ca
n be upregulated by oxidants. Oxidants can also induce the fibrogenic cytok
ine, TGF beta 1, one that is widely incriminated in progressive renal injur
y. Reduction in renal oxidative stress by dietary or pharmacologic approach
es provides an appealing target for therapies directed towards the retardat
ion of progressive renal injury.