Evidence map›Paper›PMID 33472594›Full record

ArticleBMC nephrology2021

Causal effect between total cholesterol and HDL cholesterol as risk factors for chronic kidney disease: a mendelian randomization study.

Liu Miao, Yan Min, Bin Qi, Chuan-Meng Zhu, Jian-Hong Chen, Guo-Xiong Deng, Yong Wang, Jian-Fei Li, Rong-Shan Li

Open access · goldAbstract read
In one paragraph

Article in BMC nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Liu Miao *Departments of Cardiology, Liuzhou People's Hospital, 8 Wenchang Road, Liuzhou, 545006, Guangxi, People's Republic of China. 675666690@qq.com.ORCID 0000-0001-6642-7005
Yan Min *Departments of Nephrology, Liuzhou People's Hospital, 8 Wenchang Road, Liuzhou, 545006, Guangxi, People's Republic of China.
Bin QiDepartments of Cardiology, Liuzhou People's Hospital, 8 Wenchang Road, Liuzhou, 545006, Guangxi, People's Republic of China.
Chuan-Meng ZhuDepartments of Cardiology, Liuzhou People's Hospital, 8 Wenchang Road, Liuzhou, 545006, Guangxi, People's Republic of China.
Jian-Hong ChenDepartments of Cardiology, Liuzhou People's Hospital, 8 Wenchang Road, Liuzhou, 545006, Guangxi, People's Republic of China.
Guo-Xiong DengDepartments of Cardiology, The First People's Hospital of Nanning, 89 Qixing Road, Nanning, 530022, Guangxi, People's Republic of China.
Yong WangDepartments of Cardiology, Liuzhou People's Hospital, 8 Wenchang Road, Liuzhou, 545006, Guangxi, People's Republic of China.
Jian-Fei LiDepartments of Nephrology, Liuzhou People's Hospital, 8 Wenchang Road, Liuzhou, 545006, Guangxi, People's Republic of China.
Rong-Shan LiDepartments of Cardiology, Liuzhou People's Hospital, 8 Wenchang Road, Liuzhou, 545006, Guangxi, People's Republic of China.
Liuzhou General Hospital · CNFirst People's Hospital of Nanning · CN

Funding

Guangxi self-financing research projects Z20190025
6 · The paper itself

Abstract

backgroundWhile 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.

methodsTo 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).

resultsMR 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.

conclusionsThe 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.

Indexed as

Cholesterol, HDLCholesterol, LDLHumansMendelian Randomization AnalysisRenal Insufficiency, ChronicRisk FactorsTriglyceridesCholesterol, HDLCholesterol, LDLTriglyceridesCausationChronic kidney diseaseGenome-wide association studySerum lipid levelsTwo-sample mendelian randomization

Identifiers

PMID33472594
PMCPMC7818570
OpenAlexW3113956421

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.