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Causal effect between total cholesterol and HDL cholesterol as risk factors for chronic kidney disease: a mendelian
1Departments of Cardiology, Liuzhou People's Hospital, 8 Wenchang Road, Liuzhou, 545006, Guangxi, People's Republic of China. 675666690@qq.com.
Insights
This study suggests that lower total cholesterol (TC) and higher HDL cholesterol (HDL-C) may reduce the risk of chronic kidney disease (CKD). Further research is needed to confirm these findings.
Area of Science:
- Genetics
- Nephrology
- Cardiovascular Science
Background:
- Observational studies link serum lipids to cardiovascular disease (CVD).
- Intervention studies on lipid levels and chronic kidney disease (CKD) prevention are limited.
- Understanding the causal role of lipids in CKD etiology is crucial.
Purpose of the Study:
- To investigate the causal relationship between serum lipid levels and the development of CKD.
- To estimate the impact of specific lipid fractions on CKD incidence using genetic data.
- To provide evidence for potential lipid-modulating strategies in CKD prevention.
Main Methods:
- A two-sample Mendelian randomization (MR) study was conducted.
- Genome-wide association study (GWAS) data from large consortia (GLGC, CKDGen) were utilized.
- Single nucleotide polymorphisms (SNPs) associated with total cholesterol (TC), triglycerides (TG), HDL cholesterol (HDL-C), LDL cholesterol (LDL-C), apolipoprotein A1 (ApoA1), and apolipoprotein B (ApoB) served as instrumental variables for CKD.
Main Results:
- MR analysis indicated a significant causal effect of TC on CKD (OR: 0.756, P=0.002).
- A suggestive causal effect was observed for HDL-C and CKD (OR: 0.85, P=0.049).
- No significant causal effects were found for TG, LDL-C, ApoA1, or ApoB on CKD. Sensitivity analyses supported the association of TC and HDL-C with CKD.
Conclusions:
- This MR study provides evidence for a causal link between TC, HDL-C, and CKD.
- Lowering TC and increasing HDL-C may potentially reduce CKD incidence.
- Further genetic and environmental studies are warranted to confirm these findings and explore therapeutic implications.
Background:
While observational studies show an association between serum lipid levels and cardiovascular disease (CVD), intervention studies that examine the preventive effects of serum lipid levels on the development of CKD are lacking.
Methods:
To estimate the role of serum lipid levels in the etiology of CKD, we conducted a two-sample mendelian randomization (MR) study on serum lipid levels. Single nucleotide polymorphisms (SNPs), which were significantly associated genome-wide with serum lipid levels from the GLGC and CKDGen consortium genome-wide association study (GWAS), including total cholesterol (TC, n = 187,365), triglyceride (TG, n = 177,861), HDL cholesterol (HDL-C, n = 187,167), LDL cholesterol (LDL-C, n = 173,082), apolipoprotein A1 (ApoA1, n = 20,687), apolipoprotein B (ApoB, n = 20,690) and CKD (n = 117,165), were used as instrumental variables. None of the lipid-related SNPs was associated with CKD (all P > 0.05).
Results:
MR analysis genetically predicted the causal effect between TC/HDL-C and CKD. The odds ratio (OR) and 95% confidence interval (CI) of TC within CKD was 0.756 (0.579 to 0.933) (P = 0.002), and HDL-C was 0.85 (0.687 to 1.012) (P = 0.049). No causal effects between TG, LDL-C- ApoA1, ApoB and CKD were observed. Sensitivity analyses confirmed that TC and HDL-C were significantly associated with CKD.
Conclusions:
The findings from this MR study indicate causal effects between TC, HDL-C and CKD. Decreased TC and elevated HDL-C may reduce the incidence of CKD but need to be further confirmed by using a genetic and environmental approach.
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