Evidence map›Paper›PMID 21537348›Full record

ReviewNature reviews. Nephrology2011

The population genetics of chronic kidney disease: insights from the MYH9-APOL1 locus.

Saharon Rosset, Shay Tzur, Doron M Behar, Walter G Wasser, Karl Skorecki

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 3 pooled it
4.9field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 3 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Pooled it
  4. Trial
  5. Blood pressure andClinical kidney journal · 2026
    Article
  6. Article
  7. Article
  8. Multiethnic prevalence of theClinical kidney journal · 2025
    Article
  9. Review
  10. Review
  11. Genetic Variants ofKidney international reports · 2022
    Article
  12. Kidney disease and APOL1.Human molecular genetics · 2021
    Review
  13. Association of Serum Thyroid Hormones with the Risk and Severity of Chronic Kidney Disease Among 3563 Chinese Adults.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  14. Article
  15. Article
  16. APOL1-Associated Kidney Disease in Brazil.Kidney international reports · 2019
    Article
  17. Article
  18. Article
  19. Linking Race, Cancer Outcomes, and Tissue Repair.The American journal of pathology · 2018
    Review
  20. Article
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 4 institutions in 1 country.

Saharon RossetDepartment of Statistics and Operations Research, Tel Aviv University, Tel Aviv 69978, Israel.
Shay Tzur
Doron M Behar
Walter G Wasser
Karl Skorecki
Technion – Israel Institute of Technology · ILHadassah Medical Center · ILRambam Health Care Campus · ILTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many rare kidney disorders exhibit a monogenic, Mendelian pattern of inheritance. Population-based genetic studies have identified many genetic variants associated with an increased risk of developing common kidney diseases. Strongly associated variants have potential clinical uses as predictive markers and may advance our understanding of disease pathogenesis. These principles are elegantly illustrated by a region within chromosome 22q12 that has a strong association with common forms of kidney disease. Researchers had identified DNA sequence variants in this locus that were highly associated with an increased prevalence of common chronic kidney diseases in people of African ancestry. Initial research concentrated on MYH9 as the most likely candidate gene; however, population-based whole-genome analysis enabled two independent research teams to discover more strongly associated mutations in the neighboring APOL1 gene. The powerful evolutionary selection pressure of an infectious pathogen in West Africa favored the spread of APOL1 variants that protect against a lethal form of African sleeping sickness but are highly associated with an increased risk of kidney disease. We describe the data sources, process of discovery, and reasons for initial misidentification of the candidate gene, as well as the lessons that can be learned for future population genetics research.

Indexed as

Apolipoprotein L1ApolipoproteinsGenetic Predisposition to DiseaseGenetics, PopulationHumansKidney Failure, ChronicLipoproteins, HDLMolecular Motor ProteinsMyosin Heavy ChainsPrevalenceRisk FactorsAPOL1 protein, humanApolipoprotein L1ApolipoproteinsLipoproteins, HDLMolecular Motor ProteinsMYH9 protein, humanMyosin Heavy Chains

Identifiers

PMID21537348
OpenAlexW2057221053

What OpenQuestion holds

Textmetadata
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.