Lipoprotein(a) and CKD

Lipoprotein(a) (Lp[a]) was discovered more than six decades ago. Since then, it has evolved from a subject of curious experiments performed by a few scientists to an extensively explored therapeutic target for prevention and management of cardiovascular disease (CVD). This has prompted an intense search for therapies and agents with potent Lp(a)-specific lowering effects on the horizon. Some of these agents are already in clinical trials to clarify whether lowering high Lp(a) levels would result in reductions in CVD events. The road to this point has been filled with many challenges, where landmark genetic discoveries opened new avenues and set the stage for interventions. Although there is no doubt that genetics play a key role in determining Lp(a) level, accumulating evidence also supports a role for some clinical conditions in influencing Lp(a) levels. CKD is a prevalent condition associated with elevated Lp(a) levels. Most available data show that elevated Lp(a) levels predict CVD risk in patients with CKD. Given the growing evidence for a relationship between Lp(a), CVD, and CKD as well as ongoing cardiovascular outcomes trials of Lp(a)-specific agents, we provide an overview of recent evidence on this topic. We focus on recent studies in patients with CKD on treatment modalities affecting Lp(a) level as well as on existing gaps in knowledge and future research directions related to clinical care and CVD risk reduction in patients with CKD.