Evidence map›Paper›PMID 25853332›Full record

ReviewKidney international2015

APOL1 toxin, innate immunity, and kidney injury.

Sophie Limou, Patrick D Dummer, George W Nelson, Jeffrey B Kopp, Cheryl A Winkler

Open access · greenAbstract readReview
In one paragraph

Review in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. A novelRenal failure · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Multiethnic prevalence of theClinical kidney journal · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Association betweeneLife · 2023
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Apolipoprotein L1 and mechanisms of kidney disease susceptibility.Current opinion in nephrology and hypertension · 2021
    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

5 authors at 2 institutions in 1 country.

Sophie LimouMolecular Genetic Epidemiology Section, Basic Research Laboratory, Basic Science Program, Center for Cancer Research, NCI, NIH, Leidos Biomedical Research, Frederick National Laboratory, Frederick, Maryland, USA.
Patrick D DummerKidney Disease Section, NIDDK, NIH, Bethesda, Maryland, USA.
George W NelsonCenter for Cancer Research Informatics Core, Leidos Biomedical Research, Frederick National Laboratory, Frederick, Maryland, USA.
Jeffrey B KoppKidney Disease Section, NIDDK, NIH, Bethesda, Maryland, USA.
Cheryl A WinklerMolecular Genetic Epidemiology Section, Basic Research Laboratory, Basic Science Program, Center for Cancer Research, NCI, NIH, Leidos Biomedical Research, Frederick National Laboratory, Frederick, Maryland, USA.
Leidos (United States) · USNational Institutes of Health · US

Funding

CCR Collaborative Bioinformatics ResourceZICBC011532 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MALIK, MARIAM · 2013 to 2025
$33.7M
Focal Segmental Glomerulosclerosis: Genetics & MechanismsZIADK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2009 to 2024
$15.7M
Genetics of Renal Disease in African AmericansZIABC010022 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WINKLER, CHERYL · 2009 to 2022
$8.9M
Focal segmental glomerulosclerosis: TreatmentZIADK043412 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2009 to 2024
$7.4M
IDENTIFICATION OF GENETIC MARKERS FOR FOCAL SEGMENTAL GLOMERULOSCLEROSISZ01BC010022 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WINKLER, CHERYL ANN · 1996 to 2008
$701k
Intramural NIH HHS Z01 BC010022PHS HHS HHSN26120080001E
6 · The paper itself

Abstract

The discovery that two common APOL1 alleles were strongly associated with nondiabetic kidney diseases in African descent populations led to hope for improved diagnosis and treatment. Unfortunately, we still do not have a clear understanding of the biological function played by APOL1 in podocytes or other kidney cells, nor how the renal risk alleles initiate the development of nephropathies. Important clues for APOL1 function may be gleaned from the natural defense mechanism of APOL1 against trypanosome infections and from similar proteins (e.g., diphtheria toxin, mammalian Bcl-2 family members). This review provides an update on the biological functions for circulating (trypanosome resistance) and intracellular (emerging role for autophagy) APOL1. Further, we introduce a multimer model for APOL1 in kidney cells that reconciles the gain-of-function variants with the recessive inheritance pattern of APOL1 renal risk alleles.

Indexed as

Immunity, InnateAcute Kidney InjuryAllelesApolipoprotein L1ApolipoproteinsAutophagyHumansLipoproteins, HDLTrypanosomiasisAPOL1 protein, humanApolipoprotein L1ApolipoproteinsLipoproteins, HDL

Identifiers

PMID25853332
PMCPMC4490079
OpenAlexW2004577335

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.