Lipoprotein(a) and the Risk for Recurrent Atherosclerotic Cardiovascular Events Among Adults With CKD: The Chronic Renal Insufficiency Cohort (CRIC) Study
“… 7 However, in the 2023 Chronic Renal Insufficiency Cohort Study, lipoprotein(a) was not associated with increased CVD risk, suggesting that other factors may be more important in patients with end‐stage renal disease. 87 …”
Section: Nongenetic Determinants Of Plasma Lipoprotein(a) Levelsmentioning
Elevated lipoprotein(a) is a genetically transmitted codominant trait that is an independent risk driver for cardiovascular disease. Lipoprotein(a) concentration is heavily influenced by genetic factors, including
LPA
kringle IV‐2 domain size, single‐nucleotide polymorphisms, and interleukin‐1 genotypes. Apolipoprotein(a) is encoded by the
LPA
gene and contains 10 subtypes with a variable number of copies of kringle ‐2, resulting in >40 different apolipoprotein(a) isoform sizes. Genetic loci beyond
LPA
, such as
APOE
and
APOH
, have been shown to impact lipoprotein(a) levels. Lipoprotein(a) concentrations are generally 5% to 10% higher in women than men, and there is up to a 3‐fold difference in median lipoprotein(a) concentrations between racial and ethnic populations. Nongenetic factors, including menopause, diet, and renal function, may also impact lipoprotein(a) concentration. Lipoprotein(a) levels are also influenced by inflammation since the
LPA
promoter contains an interleukin‐6 response element; interleukin‐6 released during the inflammatory response results in transient increases in plasma lipoprotein(a) levels. Screening can identify elevated lipoprotein(a) levels and facilitate intensive risk factor management. Several investigational, RNA‐targeted agents have shown promising lipoprotein(a)‐lowering effects in clinical studies, and large‐scale lipoprotein(a) testing will be fundamental to identifying eligible patients should these agents become available. Lipoprotein(a) testing requires routine, nonfasting blood draws, making it convenient for patients. Herein, we discuss the genetic determinants of lipoprotein(a) levels, explore the pathophysiological mechanisms underlying the association between lipoprotein(a) and cardiovascular disease, and provide practical guidance for lipoprotein(a) testing.
“… 7 However, in the 2023 Chronic Renal Insufficiency Cohort Study, lipoprotein(a) was not associated with increased CVD risk, suggesting that other factors may be more important in patients with end‐stage renal disease. 87 …”
Section: Nongenetic Determinants Of Plasma Lipoprotein(a) Levelsmentioning
Elevated lipoprotein(a) is a genetically transmitted codominant trait that is an independent risk driver for cardiovascular disease. Lipoprotein(a) concentration is heavily influenced by genetic factors, including
LPA
kringle IV‐2 domain size, single‐nucleotide polymorphisms, and interleukin‐1 genotypes. Apolipoprotein(a) is encoded by the
LPA
gene and contains 10 subtypes with a variable number of copies of kringle ‐2, resulting in >40 different apolipoprotein(a) isoform sizes. Genetic loci beyond
LPA
, such as
APOE
and
APOH
, have been shown to impact lipoprotein(a) levels. Lipoprotein(a) concentrations are generally 5% to 10% higher in women than men, and there is up to a 3‐fold difference in median lipoprotein(a) concentrations between racial and ethnic populations. Nongenetic factors, including menopause, diet, and renal function, may also impact lipoprotein(a) concentration. Lipoprotein(a) levels are also influenced by inflammation since the
LPA
promoter contains an interleukin‐6 response element; interleukin‐6 released during the inflammatory response results in transient increases in plasma lipoprotein(a) levels. Screening can identify elevated lipoprotein(a) levels and facilitate intensive risk factor management. Several investigational, RNA‐targeted agents have shown promising lipoprotein(a)‐lowering effects in clinical studies, and large‐scale lipoprotein(a) testing will be fundamental to identifying eligible patients should these agents become available. Lipoprotein(a) testing requires routine, nonfasting blood draws, making it convenient for patients. Herein, we discuss the genetic determinants of lipoprotein(a) levels, explore the pathophysiological mechanisms underlying the association between lipoprotein(a) and cardiovascular disease, and provide practical guidance for lipoprotein(a) testing.
Background
Serum lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerotic cardiovascular disease (ASCVD) in the general population, its association with ASCVD incidence in Chinese maintenance hemodialysis (MHD) patients remains unclear. We aimed to evaluate the relationship between Lp(a) levels and ASCVD incidence among MHD patients in Beijing, China.
Methods
This retrospective, observational cohort study included MHD patients at Beijing Tongren Hospital from January 1, 2013 to December 1, 2020, and followed until December 1,2023. The primary outcome was ASCVD occurrence. Kaplan-Meier survival analysis was used to evaluate ASCVD-free survival in MHD patients, with stratification based on Lp(a) levels. Cox regression analyses were conducted to assess the association between Lp(a) levels and the occurrence of ASCVD.
Results
A total of 265 patients were enrolled in the study. The median follow-up period were 71 months.78 (29.4%) participants experienced ASCVD events, and 118 (47%) patients died, with 58 (49.1%) deaths attributed to ASCVD. Spearman rank correlation analyses revealed positive correlations between serum Lp(a) levels and LDL-c levels, and negative correlations with hemoglobin, triglyceride, serum iron, serum creatinine, and albumin levels. Multivariate Cox regression analysis showed that Lp(a) levels ≥ 30 mg/L, increased age, decreased serum albumin levels, and a history of diabetes mellitus were significantly associated with ASCVD incidence.
Conclusions
This study demonstrated an independent and positive association between serum Lp(a) levels and the risk of ASCVD in MHD patients, suggesting that serum Lp(a) could potentially serve as a clinical biomarker for estimating ASCVD risk in this population.
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