Abstract
We now have a robust knowledge base for a role for oxidative stress and reactive oxygen and nitrogen species in the pathogenesis of kidney failure and disease. This has developed from recent advances in research, particularly from the use of new markers of oxidative stress in urine, serum, and tissue samples, in conjunction with kidney functional and structural deficit. While experimental models have, in general, been more successful in defining a role for oxidative stress in diseases of the kidney than human investigations, a variety of clinical trials has now also supported the data gained experimentally through the greatly improved diagnostic techniques. Kidney failure is the final limiting outcome of most kidney diseases and can occur short term, over days to weeks (acute kidney injury), or more insidiously over a long time (chronic kidney disease and end-stage kidney failure). A unifying hypothesis for development of these diseases is mitochondrial dysfunction, excess production of damaging reactive species, and a deficit in natural antioxidant activity. Although results from experimental models indicate benefit of boosting our natural cellular antioxidant defenses with antioxidant therapies, to date, these therapies per se have generally been disappointing in delivering renoprotection in humans. This chapter serves to address the general classifications of acute kidney injury and chronic kidney disease; indicate the function of the reactive species, particularly reactive oxygen species, in the development and progression of the diseases; present some examples of experimental and clinical studies on oxidative stress in kidney disease; and highlight some of the clinical benefits, but also the uncertainties, of antioxidant therapies.
Published Version
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