Evidence map›Paper›PMID 30340464›Full record

SynthesisBMC medical genetics2018

An African perspective on the genetic risk of chronic kidney disease: a systematic review.

Cindy George, Yandiswa Y Yako, Ikechi G Okpechi, Tandi E Matsha, Francois J Kaze Folefack, Andre P Kengne

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in BMC medical genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
1.1field-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, 2 syntheses or guidelines pooled it, 20 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

6 authors at 5 institutions in 2 countries.

Cindy GeorgeNon-Communicable Diseases Research Unit, South African Medical Research Council, Parow Valley, PO Box 19070, Cape Town, South Africa. cindy.george@mrc.ac.za.ORCID 0000-0002-4561-0529
Yandiswa Y YakoDepartment of Human Biology, Faculty of Health Sciences, Walter Sisulu University, Mthatha, South Africa.
Ikechi G OkpechiDepartment of Medicine, Division of Nephrology and Hypertension, University of Cape Town, Cape Town, South Africa.
Tandi E MatshaDepartment of Biomedical Sciences, Faculty of Health and Wellness Science, Cape Peninsula University of Technology, Bellville, Cape Town, South Africa.
Francois J Kaze FolefackFaculty of Medicine and Biomedical Sciences, University of Yaounde I, Yaounde, Cameroon.
Andre P KengneNon-Communicable Diseases Research Unit, South African Medical Research Council, Parow Valley, PO Box 19070, Cape Town, South Africa.
South African Medical Research Council · ZACape Peninsula University of Technology · ZAUniversité de Yaoundé I · CMUniversity of Cape Town · ZAWalter Sisulu University · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIndividuals of African ethnicity are disproportionately burdened with chronic kidney disease (CKD). However, despite the genetic link, genetic association studies of CKD in African populations are lacking.

methodsWe conducted a systematic review to critically evaluate the existing studies on CKD genetic risk inferred by polymorphism(s) amongst African populations in Africa. The study followed the HuGE handbook and PRISMA protocol. We included studies reporting on the association of polymorphism(s) with prevalent CKD, end-stage renaldisease (ESRD) or CKD-associated traits. Given the very few studies investigating the effects of the same single nucleotide polymorphisms (SNPs) on CKD risk, a narrative synthesis of the evidence was conducted.

resultsA total of 30 polymorphisms in 11 genes were investigated for their association with CKD, ESRD or related traits, all using the candidate-gene approach. Of all the included genes, MYH9, AT1R and MTHFR genes failed to predict CKD or related traits, while variants in the APOL1, apoE, eNOS, XPD, XRCC1, renalase, ADIPOQ, and CCR2 genes were associated with CKD or other related traits. Two SNPs (rs73885319, rs60910145) and haplotypes (G-A-G; G1; G2) of the apolipoprotein L1 (APOL1) gene were studied in more than one population group, with similar association with prevalent CKD observed. The remaining polymorphisms were investigated in single studies.

conclusionAccording to this systematic review, there is currently insufficient evidence of the specific polymorphisms that poses African populations at an increased risk of CKD. Large-scale genetic studies are warranted to better understand susceptibility polymorphisms, specific to African populations.

Indexed as

Black PeoplePolymorphism, Single NucleotideAdiponectinAllelesApolipoprotein L1Apolipoproteins EFemaleGene ExpressionGene FrequencyGenome-Wide Association StudyHaplotypesHumansKidney Failure, ChronicMaleMonoamine OxidaseNitric Oxide Synthase Type IIIAdiponectinADIPOQ protein, humanApoE protein, humanAPOL1 protein, humanApolipoprotein L1Apolipoproteins ECCR2 protein, humanERCC2 protein, humanMonoamine OxidaseNitric Oxide Synthase Type IIINOS3 protein, humanReceptors, CCR2renalaseXeroderma Pigmentosum Group D ProteinX-ray Repair Cross Complementing Protein 1XRCC1 protein, humanAfricaChronic kidney diseaseEnd-stage renal diseaseGenetics

Identifiers

PMID30340464
PMCPMC6194564
OpenAlexW2897645136

What OpenQuestion holds

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LicenceCC BY
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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.