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* Division of Nephrology, Keck School of Medicine, University of Southern California, Los Angeles, California; and
Division of Nephrology & Hypertension, University of Miami, Miami, Florida
Address correspondence to: Dr. Vito M. Campese, Department of Medicine, Physiology and Biophysics, Division of Nephrology and Hypertension Center, Keck School of Medicine, University of Southern California, 1200 North State Street, Los Angeles, CA 90033. Phone: 323-226-7337; Fax: 323-226-5390; E-mail: campese{at}usc.edu
Statins reduce serum cholesterol and cardiovascular morbidity and mortality. The mechanisms for these beneficial effects are reviewed. Altered inflammatory responses and improved endothelial function mediated by statins are thought to be partly responsible for the reduction of morbidity and mortality as a result of cardiovascular events. In analogy, whether statins confer similar benefits on the kidney has not been established. This review critically considers the available data whereby dyslipidemia mediates renal dysfunction by modulating the inflammatory response to diverse cytokines. Also reviewed is the emerging database indicating that statins may modulate renal function by altering the response of the kidney to dyslipidemia.
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