Evidence map›Paper›PMID 30343724›Full record

ReviewAmerican journal of kidney diseases : the official journal of the National Kidney Foundation2018

APOL1-Associated Nephropathy: A Key Contributor to Racial Disparities in CKD.

Barry I Freedman, Sophie Limou, Lijun Ma, Jeffrey B Kopp

Abstract readReview
In one paragraph

Review in American journal of kidney diseases : the official journal of the National Kidney Foundation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 4 pooled it
11.8field-weighted citation impact, top 1% 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

85 citing papers in PubMed, 4 syntheses or guidelines pooled it, 154 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Update on APOL1 and chronic kidney diseases in children.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Molecular Mechanisms of APOL1-Associated Kidney Disease.International journal of molecular sciences · 2026
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Observational
  19. Interaction BetweenKidney international reports · 2025
    Article
  20. Article

25 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Barry I FreedmanSection on Nephrology, Department of Internal Medicine; Wake Forest School of Medicine, Winston-Salem, NC. Electronic address: bfreedma@wakehealth.edu.
Sophie LimouCentre de Recherche en Transplantation et Immunologie (CRTI) UMR1064, INSERM, Université de Nantes, Nantes, France; Institut de Transplantation Urologie et Néphrologie (ITUN), CHU Nantes, Nantes, France; Ecole Centrale de Nantes, Nantes, France.
Lijun MaSection on Nephrology, Department of Internal Medicine; Wake Forest School of Medicine, Winston-Salem, NC.
Jeffrey B KoppKidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD. Electronic address: jbkopp@nih.gov.
Wake Forest University · USInserm · FRNational Institutes of Health · US

Funding

Focal Segmental Glomerulosclerosis: Genetics & MechanismsZIADK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2009 to 2024
$15.7M
Genetic Analysis of African American Hypertensive End-Stage Renal DiseaseR01DK070941 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI FREEDMAN, BARRY IRA · 2006 to 2015
$4.7M
Natural History of MYH9-Associated NephropathyR01DK084149 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI FREEDMAN, BARRY IRA · 2009 to 2012
$2.3M
NIDDK NIH HHS R01 DK070941NIDDK NIH HHS R01 DK084149
6 · The paper itself

Abstract

Genetic methodologies are improving our understanding of the pathophysiology in diverse diseases. Breakthroughs have been particularly impressive in nephrology, for which marked disparities exist in rates and etiologic classifications of end-stage kidney disease between African Americans and European Americans. Discovery of the apolipoprotein L1 gene (APOL1) association with focal segmental glomerulosclerosis, human immunodeficiency virus (HIV)-associated nephropathy, lupus nephritis, sickle cell nephropathy, and solidified glomerulosclerosis, as well as more rapid failure of transplanted kidneys from donors with APOL1 renal-risk genotypes, has improved our understanding of nondiabetic nephropathy. Environmental factors acting through natural selection in sub-Saharan African populations likely underlie this association. This article describes the discovery of chromosome 22q renal-risk variants and their worldwide distribution, reviews the epidemiology and pathology of APOL1-associated nephropathies, and explores several proposed mechanisms of kidney injury identified in cell culture and animal models. Detection of APOL1 associations with kidney diseases and delineation of injury pathways brings hope for effective treatment for these kidney diseases.

Indexed as

Genetic Predisposition to DiseaseMutationRacial GroupsRenal Insufficiency, ChronicApolipoprotein L1DNADNA Mutational AnalysisGlobal HealthHumansMorbidityRisk FactorsAPOL1 protein, humanApolipoprotein L1DNAAfrican AmericansAfrican ancestryAPOL1apolipoprotein A1chronic kidney disease (CKD)disparitiesfocal segmental glomerulosclerosis (FSGS)genetic determinantsgenotypeHIV-associated nephropathy (HIVAN)race/ethnicityrenal risk variantreview

Identifiers

PMID30343724
PMCPMC6200346
OpenAlexW2896700085

What OpenQuestion holds

Textmetadata
LicenceTDM
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.