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Lipoprotein(a) and Cardiovascular Risk: Emerging Therapeutic Perspectives with Implications for Chronic Kidney

Luca Di Lullo1, Paola Peverini2, Antonio Bellasi3

  • 1Department of Nephrology and Dialysis, Azienda USL Roma 6, Ariccia, Italy, dilulloluca69@gmail.com.

Cardiorenal Medicine
|July 10, 2026
PubMed

Insights

Lipoprotein(a) [Lp(a)], a genetic risk factor for cardiovascular disease, should be measured once in adulthood. New therapies lower Lp(a), but cardiovascular outcome data are pending.

Area of Science:

  • Cardiovascular Medicine
  • Genetics
  • Pharmacology

Background:

  • Lipoprotein(a) [Lp(a)] is an LDL-like particle linked to cardiovascular disease.
  • Elevated Lp(a) is a genetically determined risk factor for atherosclerotic cardiovascular disease and calcific aortic valve stenosis.
  • Lp(a) measurement is recommended for cardiovascular risk assessment, especially in individuals with suboptimal LDL-cholesterol control.

Purpose of the Study:

  • To review the role of Lp(a) in cardiovascular disease, particularly in chronic kidney disease (CKD).
  • To discuss the current understanding of Lp(a) genetics and its limited modifiability by lifestyle or conventional therapies.
  • To highlight emerging Lp(a)-lowering therapies and the need for outcome data.

Main Methods:

  • Literature review of Lp(a) in cardiovascular disease and CKD.
  • Analysis of current guidelines regarding Lp(a) measurement.
  • Overview of novel Lp(a)-lowering therapeutic strategies.

Main Results:

  • Elevated Lp(a) is an independent risk factor for cardiovascular disease and calcific aortic valve stenosis.
  • Lp(a) levels are primarily inherited and minimally affected by lifestyle or standard lipid-lowering treatments.
  • Lp(a) may increase in chronic kidney disease, contributing to cardiovascular risk, though the causal link is not fully established.

Conclusions:

  • Measuring Lp(a) is crucial for refining cardiovascular risk assessment in adults.
  • Novel therapies show promise in reducing Lp(a) levels, but clinical outcome data are essential.
  • Further research is needed to clarify the causal role of Lp(a) in CKD-related cardiovascular events.
Abstract

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