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J Am Soc Nephrol 15:901-909, 2004
© 2004 American Society of Nephrology

BASIC SCIENCE

Atorvastatin Improves the Course of Ischemic Acute Renal Failure in Aging Rats

Massimo Sabbatini*, Antonio Pisani*, Francesco Uccello*, Vittorio Serio*, Rosalba Serù{dagger}, Roberto Paternò{dagger}, Bruno Cianciaruso*, Giorgio Fuiano{ddagger} and Michele Andreucci{ddagger}

Departments of *Nephrology and {dagger}Internal Medicine, University Federico II, Naples, Italy; and {ddagger}Department of Nephrology, "Magna Graecia" University, Catanzaro, Italy.

Correspondence to Dr. Massimo Sabbatini, Department of Nephrology, University Federico II, Via A. Manzoni 50, 80123, Naples, Italy. Phone: +39-081-746-2614, Fax: +39-081-746-2149; E-mail: sabbatin{at}unina.it

ABSTRACT. Statins increase the production of nitric oxide (NO) and have beneficial effects on the course of acute renal failure (ARF) in young rats. The effects of a short-term treatment with atorvastatin (ATO) on ischemic ARF in old rats, characterized by a great susceptibility to ischemia, was tested. No difference was found in renal dynamics between young (Y, 3 mo old) and old (O, 18 mo old) rats in normal conditions (CON) or after ATO treatment (12 mg/kg/d for 14 d). Twenty-four hours after clamping of both renal arteries, a more pronounced decrease in GFR was observed in O rats versus Y rats after a greater renal vasoconstriction and hypoperfusion of aging animals. Pretreatment with ATO mitigated renal vasoconstriction in O rats and restored GFR values to Y rats. Nitrate excretion was enhanced in Y rats after ARF but was not further modified by ATO; in O rats, ARF did not increase nitrate excretion, which was raised after ATO treatment. This reflected the increase in endothelial NO synthase (eNOS)–mRNA expression and eNOS protein observed in old ATO-treated animals with ARF. ATO treatment had also a significant protective effect against the cell injury at tubular level in O, but not Y, rats. The Ras system was not influenced by ATO in O rats, whereas the activation of Rho proteins was partially inhibited by ATO. Low-dose treatment with ATO enhances NO availability in aging rats, improving renal dynamics and conferring a peculiar histologic protection at tubular level after ischemia.




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