LPA gene variants triple Lp(a) levels, and the highest Lp(a) quartile raises heart attack risk by 49% in chronic kidney disease, the CRIC Study of 3744 patients (Arterioscler Thromb Vasc Biol 2017)

Original title: Lipoprotein(a) and Risk of Myocardial Infarction and Death in Chronic Kidney Disease: Findings From the CRIC Study (Chronic Renal Insufficiency Cohort)

Arterioscler Thromb Vasc Biol · 24 August 2017 · 8

Bajaj A, Damrauer SM, Anderson AH, Xie D, Budoff MJ, Go AS, He J, Lash JP, Ojo A, Post WS, Rahman M, Reilly MP et al.

The CRIC Study (Chronic Renal Insufficiency Cohort), an ongoing prospective study of 3939 participants with chronic kidney disease, examined LPA gene variants and Lp(a) association with myocardial infarction and death in 3635 genotyped and 3744 baseline-Lp(a) participants. Carriers of the rs10455872 or rs6930542 variants had much higher median Lp(a) than non-carriers (73 vs 23 mg/dL, P<0.001; and 56 vs 22 mg/dL, P<0.001). Stratified into Lp(a) quartiles (below 9.8, 9.8 to 26.0, 26.1 to 61.3, and above 61.3 mg/dL), 315 myocardial infarctions and 822 deaths occurred over a median 7.5-year follow-up. Compared with the second (lowest-risk) quartile, the highest Lp(a) quartile carried increased risk of myocardial infarction (hazard ratio 1.49, 95% CI 1.05-2.11), death (hazard ratio 1.28, 95% CI 1.05-1.57), and the composite outcome (hazard ratio 1.29, 95% CI 1.07-1.56). The findings show elevated Lp(a) independently predicts myocardial infarction and death in adults with chronic kidney disease.

Original abstract

Objective: To investigate the effect of LPA gene variants and renal function on lipoprotein(a) [Lp(a)] levels in people with chronic kidney disease and determine the association between elevated Lp(a) and myocardial infarction and death in this setting.

Approach And Results: The CRIC Study (Chronic Renal Insufficiency Cohort) is an ongoing prospective study of 3939 participants with chronic kidney disease. In 3635 CRIC participants with genotype data, carriers of the rs10455872 or rs6930542 variants had a higher median Lp(a) level (mg/dL) compared with noncarriers (73 versus 23; P<0.001 and 56 versus 22; P<0.001, respectively). The 3744 participants (55% male and 41% non-Hispanic White) with available baseline Lp(a) levels were stratified into quartiles of baseline Lp(a) (mg/dL): <9.8, 9.8 to 26.0, 26.1 to 61.3, and >61.3. There were 315 myocardial infarctions and 822 deaths during a median follow-up of 7.5 years. The second quartile had the lowest event rate. After adjusting for potential confounders and using a Cox proportional hazards model, the highest quartile of Lp(a) was associated with increased risk of myocardial infarction (hazard ratio, 1.49; 95% confidence interval, 1.05-2.11), death (hazard ratio, 1.28; 95% confidence interval, 1.05-1.57), and the composite outcome (hazard ratio, 1.29; 95% confidence interval, 1.07-1.56) compared with the second quartile of Lp(a).

Conclusions: Among adults with chronic kidney disease, elevated Lp(a) is independently associated with myocardial infarction and death. Future studies exploring pharmacological Lp(a) reduction in this population are warranted.

Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.