Evidence map›Paper›PMID 33767059›Full record

ReviewCurrent opinion in nephrology and hypertension2021

Apolipoprotein L1 and mechanisms of kidney disease susceptibility.

Leslie A Bruggeman, John R Sedor, John F O'Toole

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 15 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Albuminuria Changes as a surrogate endpoint inmedRxiv : the preprint server for health sciences · 2026
    Article
  5. Article
  6. A novelRenal failure · 2025
    Article
  7. Review
  8. Kidney medicine · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Apolipoprotein L1 (APOL1) cation current in HEK-293 cells and in human podocytes.Pflugers Archiv : European journal of physiology · 2023
    Article
  13. Review
  14. Article
  15. Clinical journal of the American Society of Nephrology : CJASN · 2021
    Article
  16. 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

3 authors at 2 institutions in 1 country.

Leslie A BruggemanDepartments of Nephrology and Inflammation & Immunity, Cleveland Clinic.
John R SedorDepartments of Nephrology and Inflammation & Immunity, Cleveland Clinic.
John F O'TooleDepartments of Nephrology and Inflammation & Immunity, Cleveland Clinic.
Cleveland Clinic · USUniversity School · US

Funding

Intracellular functions of APOL1 in the kidneyR01DK127638 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI BRUGGEMAN, LESLIE A, O'TOOLE, JOHN F. · 2021 to 2025
$2.8M
Mechanisms of APOL1-mediated kidney diseaseR01DK108329 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI BRUGGEMAN, LESLIE A, O'TOOLE, JOHN F. · 2015 to 2019
$2.0M
Kidney disease mechanisms associated with human genetic variationR01DK097836 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI BRUGGEMAN, LESLIE A, O'TOOLE, JOHN F. · 2014 to 2017
$2.0M
Viral causes of idiopathic chronic kidney diseaseR21AI135434 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI BRUGGEMAN, LESLIE A · 2018 to 2019
$440k
Kidney disease mechanisms associated with human genetic variationR56DK097836 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI BRUGGEMAN, LESLIE A, O'TOOLE, JOHN F. · 2012 to 2012
$198k
Intracellular functions of APOL1 in the kidneyR56DK127638 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI BRUGGEMAN, LESLIE A, O'TOOLE, JOHN F. · 2020 to 2020
$105k
NIAID NIH HHS R21 AI135434NIDDK NIH HHS R01 DK097836NIDDK NIH HHS R01 DK108329NIDDK NIH HHS R01 DK127638NIDDK NIH HHS R56 DK097836NIDDK NIH HHS R56 DK127638
6 · The paper itself

Abstract

purpose of reviewAllelic variants in the gene for apolipoprotein L1 (APOL1), found only in individuals of African ancestry, explain a majority of the excess risk of kidney disease in African Americans. However, a clear understanding how the disease-associated APOL1 variants cause kidney injury and the identity of environmental stressors that trigger the injury process have not been determined. RECENT

findingsBasic mechanistic studies of APOL1 biochemistry and cell biology, bolstered by new antibody reagents and inducible pluripotent stem cell-derived cell systems, have focused on the cytotoxic effect of the risk variants when APOL1 gene expression is induced. Since the APOL1 variants evolved to alter a key protein-protein interaction with the trypanosome serum resistance-associated protein, additional studies have begun to address differences in APOL1 interactions with other proteins expressed in podocytes, including new observations that APOL1 variants may alter podocyte cytoskeleton dynamics. SUMMARY: A unified mechanism of pathogenesis for the various APOL1 nephropathies still remains unclear and controversial. As ongoing studies have consistently implicated the pathogenic gain-of-function effects of the variant proteins, novel therapeutic development inhibiting the synthesis or function of APOL1 proteins is moving toward clinical trials.

Indexed as

Apolipoprotein L1Kidney DiseasesDisease SusceptibilityGenetic Predisposition to DiseaseHumansPodocytesAPOL1 protein, humanApolipoprotein L1

Identifiers

PMID33767059
PMCPMC8211384
OpenAlexW3139004505

What OpenQuestion holds

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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.