Effect of atorvastatin of the treatment of hypercholesterolemia after renal transplantation

Cardiovascular disease is a frequent cause of morbidity and mortality in renal allograft recipients. Hyperlipidemia is one of the most important factors for the development and progression of the vascular disease in these patients. In addition there is emerging evidence linking elevated lipid levels to pathogenesis of chronic allograft dysfunction.

The posttransplant lipoprotein profile is characterized by an increase in serum total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), very low density lipoprotein cholesterol (VLDL-C), and triglycerides (TG), with a normal or decreased high density lipoprotein cholesterol (HDL-C). The potential causes of hyperlipidemia include diet, genetic predisposition, immunosuppressive agents such as cyclosporine (CsA) and corticosteroids, antihypertensive or diuretic drugs, proteinuria, allograft dysfunction, and glucose intolerance. In most patients, dietary modifications are as the only form of therapy disappointing, and they usually require pharmacologic intervention. The HMG-CoA reductase inhibitors, or statins, are the most powerful agents for lowering TC and LDL-C and the most recommended for efficiency and safety in the transplant population.

Statins may also protect graft function or decelerate the atherosclerotic process through mechanisms other than cholesterol reduction by inhibition of chemotaxis of monocytes and decreasing natural killer cell cytotoxicity. The aim of this study was to evaluate the effect of atorvastatin (AT) in the treatment of hypercholesterolemia after renal transplantation.

CITATION Transplant Proc. 1999 Sep;31(6):2328-9