Cyclosporine A nephrotoxicity: Role of oxidative stress
Keywords:
Cyclosporine A, nephrotoxicity, oxidative stress, mitochondriaAbstract
Cyclosporine A (CsA) is a calcineurin inhibitor which has remained for many years a crucial immunosuppressant with a major therapeutic role in a solid organ transplantation and in various immunological diseases. The main adverse effect of CsA is nephrotoxicity. Cs-A induced kidney dysfunction and morphological damage has multifactorial pathogenesis. The renin-angiotensin system, endothelin and eicosanoids have been considered as potential mediators of CsA-related kidney dysfunction. Recently oxidative stress and reactive oxygen species (ROS) release have been proposed as an alternate source of CsA-dependent kidney damage. CsA nephrotoxicity is associated with imbalanced red-ox state and oxidative stress in renal tubular, endothelial and glomerular cells. CsA-induced ROS release in the kidney is accompanied be development of morphologic changes including vascular injury with ischemic damage, interstitial fibrosis, progressive glomerular sclerosis, tubular atrophy and cell apoptosis.
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