HMG-CoA reductase inhibitors and the kidney.

During the last two decades, numerous studies have demonstrated that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) diminish the risk of cardiovascular morbidity and mortality. Although these studies have focused primarily on the ability of statins to lower circulating levels of low-density lipoprotein cholesterol, more recent research has shown that statins may protect the vasculature via pleiotropic effects not directly related to lipid lowering. These include adjustments in cell-signaling pathways that play a role in atherogenesis and that affect the expression of inflammatory elements, curtail oxidative stress, and enhance endothelial function. More recently, researchers have begun to explore whether these agents exert similar beneficial effects in renal parenchymal and renovascular disease. This review examines the available evidence that dyslipidemia may augment the inflammatory reaction of cytokines in patients with renal disease and that statins may improve renal dysfunction by altering the response of the kidney to dyslipidemia, even in persons with end-stage renal disease on dialysis or with renal transplantation. In this context, some data suggest that statin-mediated alterations in inflammatory responses and endothelial function may reduce proteinuria and the rate of progression of kidney disease.