Evidence map›Paper›PMID 37113494›Full record

ReviewGlomerular diseases

APOL1 and APOL1-Associated Kidney Disease: A Common Disease, an Unusual Disease Gene - Proceedings of the Henry Shavelle Professorship.

Martin R Pollak, David J Friedman

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Glomerular diseases. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

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

  1. Pooled it
  2. Trial
  3. Update on APOL1 and chronic kidney diseases in children.Pediatric nephrology (Berlin, Germany) · 2026
    Review
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  5. Blood pressure andClinical kidney journal · 2026
    Article
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  20. Kidney medicine · 2025
    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

2 authors.

Martin R PollakDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.
David J FriedmanDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Genetic variants in APOL1 are a major contributor to the increased risk of kidney disease in people of recent African ancestry. Summary: Two alleles in the APOL1 gene, referred to as G1 and G2, confer increased risk of kidney disease under a recessive model of risk inheritance. Disease risk is inherited as a recessive trait: People with genotypes G1/G1, G2/G2, and G1/G2 (i.e., a risk allele from each parent) have increased risk for what we refer to here as APOL1-associated kidney disease. In the USA, about 13% of the self-identified African-American population has a high-risk genotype. As we discuss below, APOL1 is an unusual disease gene. Most studies to date have suggested that the G1 and G2 variants have toxic, gain-of-function effects on the encoded protein. Key Message: In this article, we review key concepts critical to understanding APOL1-associated kidney disease, emphasizing ways in which it is highly atypical for a human disease-causing gene.

Indexed as

APOL1FSGSGeneticKidney

Identifiers

PMID37113494
PMCPMC10126737

What OpenQuestion holds

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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.