Evidence map›Paper›PMID 36767251›Full record

ArticleInternational journal of environmental research and public health2023

Chronic Kidney Disease: Combined Effects of Gene Polymorphisms of Tissue Inhibitors of Metalloproteinase 3, Total Urinary Arsenic, and Blood Lead Concentration.

Ying-Chin Lin, Ya-Li Huang, Horng-Sheng Shiue, Sheng-Lun Hsu, Yu-Mei Hsueh

Open access · goldAbstract read
In one paragraph

Article in International journal of environmental research and public health, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 53% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Review
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

5 authors at 3 institutions in 1 country.

Ying-Chin LinDepartment of Family Medicine, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0002-1569-0169
Ya-Li HuangDepartment of Public Health, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
Horng-Sheng ShiueDepartment of Chinese Medicine, College of Medicine, Chang Gung University, Taoyuan 333, Taiwan.
Sheng-Lun HsuDepartment of Family Medicine, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan.
Yu-Mei HsuehDepartment of Family Medicine, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0001-6113-9936
Wan Fang Hospital · TWChang Gung University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tissue inhibitor of metalloproteinase 3 (TIMP3) is known to be an anti-fibrotic factor. Arsenic, lead, and cadmium exposure and selenium intake may affect TIMP3 expression. The downregulation of TIMP3 expression is related to kidney fibrosis. Genotypes of TIMP3 are related to hypertension and cardiovascular diseases. Therefore, this study explored whether TIMP3 polymorphism is associated with hypertension-related chronic kidney disease (CKD). In addition, the combined effects of TIMP3 polymorphism and total urinary arsenic, blood lead and cadmium, and plasma selenium concentrations on CKD, were investigated. This was a case-control study, with 213 CKD patients and 423 age- and sex-matched controls recruited. Polymerase chain reaction-restriction fragment length polymorphism was used to determine TIMP3 gene polymorphisms. The concentrations of urinary arsenic species, plasma selenium, and blood lead and cadmium were measured. The odds ratio (OR) of CKD in the TIMP3rs9609643 GA/AA genotype was higher than that of the GG genotype at high levels of total urinary arsenic and blood lead; the OR and 95% confidence interval (CI) were 0.57 (0.31-1.05) and 0.52 (0.30-0.93), respectively, after multivariate adjustment. High blood lead levels tended to interact with the TIMP3rs9609643 GG genotype to increase the OR of CKD, and gave the highest OR (95% CI) for CKD of 5.97 (2.60-13.67). Our study supports a possible role for the TIMP3rs9609643 risk genotype combined with high total urinary arsenic or with high blood lead concentration to increase the OR of CKD.

Indexed as

ArsenicRenal Insufficiency, ChronicSeleniumCadmiumCase-Control StudiesHumansLeadPolymorphism, GeneticTissue Inhibitor of Metalloproteinase-3ArsenicCadmiumLeadSeleniumTIMP3 protein, humanTissue Inhibitor of Metalloproteinase-3blood leadchronic kidney diseasepolymorphismstissue inhibitor of metalloproteinase 3total urinary arsenic

Identifiers

PMID36767251
PMCPMC9914449
OpenAlexW4317502653

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Registered trials

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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.