Genetics
German Chronic Kidney Disease study finds each 10 mg/dL rise in Lp(a) independently raises cardiovascular risk in 5,043 CKD patients (J Intern Med 2024)
Original title: Lipoprotein(a) concentrations and cardiovascular disease in patients with chronic kidney disease: Results from the German Chronic Kidney Disease study
In 5,043 European-ancestry participants of the German Chronic Kidney Disease (GCKD) study with an estimated GFR of 30-60 mL/min/1.73 m2, or above 60 with overt albuminuria, followed for 6.5 years, each 10 mg/dL higher Lp(a) was associated with 1.065-fold higher odds of prevalent cardiovascular disease (1,290 events, 95% CI 1.042-1.088, p < 0.001). Risk was significantly higher at Lp(a) 50 mg/dL or above, most pronounced at 70 mg/dL or above (odds ratio 1.775, 95% CI 1.409-2.231, p < 0.001) versus below 30 mg/dL. Each 10 mg/dL increment and Lp(a) at or above 70 mg/dL also increased risk of incident 3-point major adverse cardiovascular events (474 events; hazard ratio 1.037, 95% CI 1.009-1.067, p = 0.009, and hazard ratio 1.335, 95% CI 1.001-1.781, p = 0.050, respectively), with similar results for 4-point MACE (653 events). Analyses using apo(a) isoforms and genetically predicted Lp(a) yielded even stronger associations. Elevated and genetically determined Lp(a) independently predicts cardiovascular disease in mild-to-severe CKD, beyond traditional risk factors.
Original abstract
Background: Lipoprotein(a) (Lp(a)) is a causal, genetically determined risk factor for cardiovascular disease (CVD) in the general population. Patients with chronic kidney disease (CKD) have an increased CVD risk and elevated Lp(a) concentrations. Only a few studies on Lp(a) were performed in persons with mild-to-moderate CKD; none of them used genetic variants to explore potential causal associations.
Objectives: This study aims to investigate the association of measured and genetically predicted Lp(a) concentrations on prevalent and incident CVD events in the German Chronic Kidney Disease (GCKD) study.
Methods: The study included 5043 participants of European ancestry with an estimated glomerular filtration rate (eGFR) between 30 and 60 mL/min/1.73 m2 or an eGFR >60 mL/min/1.73 m2 in the presence of overt albuminuria with a follow-up of 6.5 years.
Results: With each 10 mg/dL higher Lp(a) concentration, odds for prevalent CVD (1290 events) increased 1.065-fold (95%CI: 1.042-1.088, p < 0.001). The risk was significantly higher in patients with Lp(a) ≥50 mg/dL but most pronounced in Lp(a) ≥70 mg/dL (odds ratio = 1.775 [1.409-2.231], p < 0.001) compared to Lp(a) <30 mg/dL. Each 10 mg/dL higher Lp(a) concentration and Lp(a) ≥70 mg/dL increased the risk for incident 3-point major adverse cardiovascular events (MACEs) (474 events): hazard ratio [HR] = 1.037 [1.009-1.067], p = 0.009 and HR = 1.335 [1.001-1.781], p = 0.050), respectively. Similar results were obtained for 4-point MACE (653 events). Analyses based on apo(a) isoforms and genetically predicted Lp(a) concentrations led to even stronger associations.
Conclusions: In patients with mild-to-severe CKD, elevated Lp(a) concentrations and genetic determinants of Lp(a) concentrations are significantly associated with CVD at baseline and during follow-up, independent of traditional risk factors.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.