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      New insights into the pathophysiology of cyclosporine nephrotoxicity: a role of aldosterone.

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          Abstract

          Cyclosporine A (CsA), a calcineurin inhibitor, has improved allograft survival in solid organ transplantation and has been increasingly applied in the management of autoimmune diseases. While marked progress has been made in patient and allograft survival rates, clinical use of CsA is often limited by its nephrotoxic effect, which can be presented as two distinct and well-characterized forms: acute and chronic nephrotoxicity. The acute form is characterized by renal vasoconstriction, induced by an imbalance of vasoactive substances release, which leads to renal dysfunction. This form is reversible. The chronic toxicity, in contrast, is characterized by the vasoconstriction plus the development of structural damage that includes arteriolopathy and tubulointerstitial fibrosis that are often not reversible. The exact mechanisms of these deleterious effects are not fully understood, but major advances have occurred over the last few years. Here we review the current literature regarding the pathogenesis and strategies that have been used to ameliorate renal injury in chronic CsA nephrotoxicity. Recent observations suggest that aldosterone plays a central role in the pathogenesis of CsA nephrotoxicity and that spironolactone could be a useful agent to prevent it. These studies and the use of mineralocorticoid receptor blockade are discussed.

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          Author and article information

          Journal
          Am J Physiol Renal Physiol
          American journal of physiology. Renal physiology
          American Physiological Society
          1931-857X
          1522-1466
          Jul 2007
          : 293
          : 1
          Affiliations
          [1 ] Molecular Physiology Unit, Universidad Nacional Autónoma de México, 14000 México City, Mexico. nab@biomedicas.unam.mx
          Article
          00072.2007
          10.1152/ajprenal.00072.2007
          17429034
          ad1b54d2-8555-4213-9024-710aff179927
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