Evidence map›Paper›PMID 28732083›Full record

ArticlePloS one2017

APOL1 risk alleles among individuals with CKD in Northern Tanzania: A pilot study.

John W Stanifer, Francis Karia, Venance Maro, Kajiru Kilonzo, Xuejun Qin, Uptal D Patel, Elizabeth R Hauser

Abstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Kidney international reports · 2022
    Article
  3. Article
  4. Apolipoprotein L1 nephropathies: 2017 in review.Current opinion in nephrology and hypertension · 2018
    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

7 authors.

John W StaniferDepartment of Medicine, Duke University; Durham, NC United States of America.ORCID http://orcid.org/0000-0001-6379-300X
Francis KariaKilimanjaro Christian Medical College; Moshi, Tanzania.
Venance MaroKilimanjaro Christian Medical College; Moshi, Tanzania.
Kajiru KilonzoKilimanjaro Christian Medical College; Moshi, Tanzania.
Xuejun QinDuke Molecular Physiology Institute, Duke University School of Medicine; Durham NC United States of America.
Uptal D PatelDepartment of Medicine, Duke University; Durham, NC United States of America.
Elizabeth R HauserDepartment of Medicine, Duke University; Durham, NC United States of America.

Funding

Vanderbilt-Emory-Cornell-Duke Consortium for Global Health Fellows (VECDor)R25TW009337 · FIC · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HEIMBURGER, DOUGLAS CORBETT, VERMUND, STEN H. · 2012 to 2016
$6.3M
Renal Genomics CoreP30DK096493 · NIDDK · DUKE UNIVERSITY · PI FOSTER, MARY H., SVETKEY, LAURA P · 2012 to 2016
$5.9M
FIC NIH HHS R25 TW009337NIDDK NIH HHS P30 DK096493
6 · The paper itself

Abstract

introductionIn sub-Saharan Africa, approximately 100 million people have CKD, yet genetic risk factors are not well-understood. Despite the potential importance of understanding APOL1 risk allele status among individuals with CKD, little genetic research has been conducted. Therefore, we conducted a pilot study evaluating the feasibility of and willingness to participate in genetic research on kidney disease, and we estimated APOL1 risk allele frequencies among individuals with CKD.

methodsIn 2014, we conducted a community-based field study evaluating CKD epidemiology in northern Tanzania. We assessed for CKD using urine albumin and serum creatinine to estimate GFR. We invited participants with CKD to enroll in an additional genetic study. We obtained dried-blood spots on filter cards, from which we extracted DNA using sterile punch biopsies. We genotyped for two single nucleotide polymorphisms (SNPs) defining the APOL1 G1 risk allele and an insertion/deletion polymorphism defining the G2 risk allele. Genotyping was performed in duplicate.

resultsWe enrolled 481 participant, 57 (12%) of whom had CKD. Among these, enrollment for genotyping was high (n = 48; 84%). We extracted a median of 19.4 ng of DNA from each dried-blood spot sample, and we genotyped the two APOL1 G1 SNPs and the APOL1 G2 polymorphism. Genotyping quality was high, with all duplicated samples showing perfect concordance. The frequency of APOL1 risk variants ranged from 7.0% to 11.0%, which was similar to previously-reported frequencies from the general population of northern Tanzania (p>0.2). DISCUSSION: In individuals with CKD from northern Tanzania, we demonstrated feasibility of genotyping APOL1 risk alleles. We successfully genotyped three risk variants from DNA extracted from filter cards, and we demonstrated a high enrollment for participation. In this population, more extensive genetic studies of kidney disease may be well-received and will be feasible.

Indexed as

AdolescentAdultAllelesApolipoprotein L1ApolipoproteinsCross-Sectional StudiesFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeHumansLipoproteins, HDLMaleMiddle AgedPilot ProjectsPolymorphism, Single NucleotideAPOL1 protein, humanApolipoprotein L1ApolipoproteinsLipoproteins, HDL

Identifiers

PMID28732083
PMCPMC5521837

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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.