Key result
Elevated Lp(a) causes cardiovascular disease, but novel lowering therapies still lack definitive outcome data.
Elevated Lp(a) is a causal risk factor for cardiovascular disease, and while novel therapies show marked Lp(a)-lowering effects, definitive cardiovascular outcome data are still pending.
Lipoprotein(a) [Lp(a)] is an LDL-like particle containing apolipoprotein B100 covalently bound to apolipoprotein(a). Elevated Lp(a) is now recognized as a genetically determined, independent, and likely causal risk factor for atherosclerotic cardiovascular disease, calcific aortic valve stenosis, and residual cardiovascular risk despite optimal LDL-cholesterol control. Current European and North American recommendations support measuring Lp(a) at least once in adulthood, particularly for cardiovascular risk refinement. Lp(a) levels are predominantly inherited and are only modestly influenced by lifestyle or conventional lipid-lowering therapies. Chronic kidney disease represents a clinically relevant setting in which Lp(a) levels may rise as renal function declines and may contribute to the excess cardiovascular burden. However, the causal role of Lp(a) in CKD-related cardiovascular disease remains incompletely defined. Novel RNA-based and small-molecule therapies, including pelacarsen, olpasiran, lepodisiran, zerlasiran, and muvalaplin, have shown marked Lp(a)-lowering effects, but definitive cardiovascular outcome data are still missing.
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Lullo et al. (2026) conducted a review in Elevated Lipoprotein(a) and Chronic Kidney Disease. Elevated Lipoprotein(a) was evaluated. Elevated Lipoprotein(a) is a causal risk factor for cardiovascular disease, but definitive cardiovascular outcome data for novel Lp(a)-lowering therapies are still missing.
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