The proteinuria associated with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors is composed of primarily low-molecular weight proteins that disappear rapidly following discontinuation of the statin agent. More importantly, no evidence exists of nephrotoxicity or reduced renal function observed with the approved clinical dosages of any available statins. Recent clinical studies have suggested actual improvement in renal function demonstrated by decreases in creatinine concentrations and improvement in estimated glomerular filtration rates with both short-term and long-term administration of these agents. The progressive fibrosis and renal scarring of chronic kidney disease appears to be the end result of increased protein traffic in the proximal renal tubule. Early animal and recent clinical studies have suggested that treatment with statin agents in established chronic kidney disease can, in fact, provide renoprotection over and above that observed with aggressive blood pressure control and the use of angiotensin II antagonists.