Lipoprotein(a): a potential target for the reduction of residual cardiovascular risk in patients with chronic kidney disease.

Epidemiological evidence demonstrates that atherosclerotic cardiovascular disease (ASCVD) is a major cause of death and disability in patients with chronic kidney disease (CKD). From the early stages of CKD, and in addition to specifically related conditions, the coexistence of traditional risk factors contributes to a process of accelerated atherosclerosis. In patients with CKD, increased cardiovascular risk persists even after correction of hypertension, dyslipidemia, and diabetes, indicating a residual risk likely related to additional subtle factors. Lipoprotein(a) [Lp(a)] is an LDL-like particle containing apoB100 covalently linked to apo(a) and is now recognized as a genetically determined risk factor for ASCVD. Following its initial description, Lp(a) aroused extraordinary interest, which then waned in the late-1990s due to the controversial results of some prospective studies and the lack of effective interventions to reduce its circulating levels. Over the past two decades, clinical studies have provided robust evidence supporting the causal and independent contribution of Lp(a) to ASCVD, also suggesting a significant contribution to residual cardiovascular risk. This contribution may be particularly significant in patients with CKD, who exhibit elevated Lp(a) levels from the earliest stages of disease. The recent development of potent Lp(a)-lowering drugs offers an exciting opportunity to effectively address residual risk in the general population and in patients with CKD. No data are yet available on their use in patients with CKD but pending future definition of their efficacy on cardiovascular outcomes, approval, dosing, and long-term safety, these drugs might possibly represent a useful tool for cardiovascular prevention in these patients.