That reactive oxygen species are involved in progressive renal injury is supported by several lines of evidence: increased generation of oxidants occurs in chronic renal injury; various antioxidant strategies exert beneficial effects in models of chronic renal injury; and, oxidative stress can induce changes in the otherwise unmanipulated kidney that resemble those seen in chronic renal disease. Oxidants may contribute to progressive renal disease by virtue of their renal haemodynamic actions, by impairing glomerular permselective properties, by inducing inordinate or aberrant growth responses, by inducing loss of cellular phenotype and apoptosis, and finally, by promoting acute and chronic inflammatory responses. Certain adhesion molecules and proinflammatory mediators, and the transcription factor NFκB, can be upregulated by oxidants. Oxidants can also induce the fibrogenic cytokine, TGFβ1, one that is widely incriminated in progressive renal injury. Reduction in renal oxidative stress by dietary or pharmacologic approaches provides an appealing target for therapies directed towards the retardation of progressive renal injury.