Purpose of review: This review will examine advances in our understanding of the association between high-density lipoprotein (HDL) function and cardiovascular disease (CVD) in patients with chronic kidney disease (CKD).
Recent findings: Large randomized statin trials and related meta-analyses confirm that lipid-lowering therapy benefits patients with mild to moderate CKD, leaving a degree of residual cardiovascular risk similar to that documented in the general population. However, patients with advanced CKD on dialysis show little to no cardiovascular benefits from lipid-lowering therapy and have an exaggerated residual cardiovascular risk. HDL quantity and functionality may explain some of the residual risk. CKD modulates the level, composition and functionality of HDL, including impaired cholesterol acceptor function and pro-inflammatory effects. Although these abnormalities prevail in CKD, they do not track together and thus support the idea of separate and distinct mechanistic pathways for each of these critical functions of HDL.
Summary: CKD-induced perturbations in HDL composition, metabolism and functionality may contribute to the excess CVD in patients with CKD and present new therapeutic targets for intervention in this population.