Hyperlipidemia as a risk factor for progression of CKD in nondiabetics

Abstract

Cardiovascular disease (CVD) is the main cause of death in patients with end-stage renal disease (ESRD). Simultaneously, dyslipidemia has been recognized as an important cardiovascular risk factor in the general population, as well as in patients with chronic kidney disease (CKD). Several lines of evidence suggest that mechanisms and factors contributing to the pathogenesis of both cardiovascular and kidney injury may be similar. Moreover, abnormalities in lipid metabolism may be associated with the progression of CKD. Therefore, numerous experimental and clinical studies were conducted to assess the potential nephroprotective effects of statins. Although experimental data suggested that statins may slow down progression of CKD, which may underline the role of lipids in the pathogenesis of progression of CKD, at the present time, there is no clinical evidence indicating that statins postpone a decline in renal function. Further prospective, randomized, controlled studies designed specifically for the CKD population are needed to investigate the association between the lipids and the use of statins and CKD in particular. Despite clear evidence that lipid-lowering therapy reduces the risk of atherosclerotic events and death of cardiac causes in individuals without CKD, the use of HMG-Co-A reductase inhibitors (statins) in patients with kidney disease is significantly less frequent. For a long time one of the explanations was the lack of a prospective, randomized, controlled study designed specifically for nondialyzed CKD patients. After recent publication of the data from the SHARP trial, given the safety and potential efficacy of statins, this lipid-lowering treatment should be administered more frequently to individuals with CKD stage 1–4, as well as those undergoing dialysis.