The evidence that lipid disorders in patients following renal transplantation play a major role in the pathogenesis of atherosclerosis and chronic renal allograft rejection is circumstantial. The absolute rate of clinical vascular disease and cardiovascular complications in transplant patients, the high prevalence of an atherogenic lipid profile and the evidence from the large HMG-CoA reductase inhibitor (statin) regression trials in the general population suggest that lipid lowering treatment is necessary in most patients after renal transplantation. Furthermore, animal models and observational studies in patients have found correlations between plasma lipid levels and both acute and chronic rejection. Animal transplant models and clinical trials in heart transplant patients also suggest that statin treatment decrease the incidence of chronic rejection in a manner that may also be independent of lipid lowering. Although the mechanisms behind this protective effect remains unclear, statins may be the first agents to be effective in preventing chronic rejection and in reducing the rate of cardiovascular complication in renal transplant recipients.