Evidence map›Paper›PMID 30863424›Full record

ArticleFrontiers in genetics2019

Association of Candidate Gene Polymorphisms With Chronic Kidney Disease: Results of a Case-Control Analysis in the Nefrona Cohort.

Joan Valls, Serafí Cambray, Carles Pérez-Guallar, Milica Bozic, Marcelino Bermúdez-López, Elvira Fernández, Àngels Betriu, Isabel Rodríguez, José M Valdivielso

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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  8. CYP24A1 and KL polymorphisms are associated with the extent of vascular calcification but do not improve prediction of cardiovascular events.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2021
    Article
  9. Review
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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 3 institutions in 1 country.

Joan VallsBiostatistics Unit, Institut de Recerca Biomèdica de Lleida and Redes - Instituto de Salud Carlos III, Lleida, Spain.
Serafí CambrayVascular and Renal Translational Research Group, Biomedical Research Institute, Institut de Recerca Biomèdica de Lleida and RedinRen-ISCIII, Lleida, Spain.
Carles Pérez-GuallarBiostatistics Unit, Institut de Recerca Biomèdica de Lleida and Redes - Instituto de Salud Carlos III, Lleida, Spain.
Milica BozicVascular and Renal Translational Research Group, Biomedical Research Institute, Institut de Recerca Biomèdica de Lleida and RedinRen-ISCIII, Lleida, Spain.
Marcelino Bermúdez-LópezVascular and Renal Translational Research Group, Biomedical Research Institute, Institut de Recerca Biomèdica de Lleida and RedinRen-ISCIII, Lleida, Spain.
Elvira FernándezVascular and Renal Translational Research Group, Biomedical Research Institute, Institut de Recerca Biomèdica de Lleida and RedinRen-ISCIII, Lleida, Spain.
Àngels BetriuVascular and Renal Translational Research Group, Biomedical Research Institute, Institut de Recerca Biomèdica de Lleida and RedinRen-ISCIII, Lleida, Spain.
Isabel RodríguezBone and Mineral Research Unit, RedinRen-ISCIII, Hospital Universitario Central de Asturias, Instituto de Investigación Sanitaria del Principado de Asturias, Universidad de Oviedo, Oviedo, Spain.
José M ValdivielsoVascular and Renal Translational Research Group, Biomedical Research Institute, Institut de Recerca Biomèdica de Lleida and RedinRen-ISCIII, Lleida, Spain.
Biomedical Research Institute of Lleida · ESInstituto de Salud Carlos III · ESUniversidad de Oviedo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a major risk factor for end-stage renal disease, cardiovascular disease and premature death. Despite classical clinical risk factors for CKD and some genetic risk factors have been identified, the residual risk observed in prediction models is still high. Therefore, new risk factors need to be identified in order to better predict the risk of CKD in the population. Here, we analyzed the genetic association of 79 SNPs of proteins associated with mineral metabolism disturbances with CKD in a cohort that includes 2,445 CKD cases and 559 controls. Genotyping was performed with matrix assisted laser desorption ionization-time of flight mass spectrometry. We used logistic regression models considering different genetic inheritance models to assess the association of the SNPs with the prevalence of CKD, adjusting for known risk factors. Eight SNPs (rs1126616, rs35068180, rs2238135, rs1800247, rs385564, rs4236, rs2248359, and rs1564858) were associated with CKD even after adjusting by sex, age and race. A model containing five of these SNPs (rs1126616, rs35068180, rs1800247, rs4236, and rs2248359), diabetes and hypertension showed better performance than models considering only clinical risk factors, significantly increasing the area under the curve of the model without polymorphisms. Furthermore, one of the SNPs (the rs2248359) showed an interaction with hypertension, being the risk genotype affecting only hypertensive patients. We conclude that 5 SNPs related to proteins implicated in mineral metabolism disturbances (Osteopontin, osteocalcin, matrix gla protein, matrix metalloprotease 3 and 24 hydroxylase) are associated to an increased risk of suffering CKD.

Indexed as

chronic kidney diseasegenetic association studyhaplotypelinkage disequilibriumrisk factorssingle nucleotide polymorphism

Identifiers

PMID30863424
PMCPMC6399120
OpenAlexW2917554042

What OpenQuestion holds

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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.