Evidence map›Paper›PMID 30371607›Full record

ReviewTransplantation2019

Mechanisms of Injury in APOL1-associated Kidney Disease.

Lijun Ma, Jasmin Divers, Barry I Freedman

Abstract readReview
In one paragraph

Review in Transplantation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. A novelRenal failure · 2025
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Novel Therapies inKidney international reports · 2023
    Review
  9. Review
  10. Review
  11. Article
  12. Frontiers in genetics · 2022
    Article
  13. Clinical journal of the American Society of Nephrology : CJASN · 2021
    Article
  14. Article
  15. Apolipoprotein L1 and mechanisms of kidney disease susceptibility.Current opinion in nephrology and hypertension · 2021
    Review
  16. Kidney disease and APOL1.Human molecular genetics · 2021
    Review
  17. A focus on the association of Apol1 with kidney disease in children.Pediatric nephrology (Berlin, Germany) · 2021
    Review
  18. Article
  19. Article
  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

3 authors at 2 institutions in 1 country.

Lijun MaDepartment of Internal Medicine, Section on Nephrology, Wake Forest School of Medicine, Winston-Salem, NC.
Jasmin DiversDivision of Public Health Sciences, Department of Biostatistical Sciences.
Barry I FreedmanDepartment of Internal Medicine, Section on Nephrology, Wake Forest School of Medicine, Winston-Salem, NC.
Wake Forest University · USBiostatistical Consulting (United States) · US

Funding

Wake Forest APOLLO Scientific and Data Research CenterU01DK116041 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Nicholette D. Allred, BARRY Ira FREEDMAN · 2017 to 2026
$8.7M
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
Genetic Determinants of Renal Transplant Survival from African American DonorsR01MD009055 · NIMHD · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DIVERS, JASMIN, FREEDMAN, BARRY IRA · 2014 to 2018
$2.0M
NIDDK NIH HHS R01 DK070941NIDDK NIH HHS R01 DK084149NIDDK NIH HHS U01 DK116041NIMHD NIH HHS R01 MD009055
6 · The paper itself

Abstract

backgroundAn improved understanding of the pathogenesis in apolipoprotein L1 (APOL1) gene-associated chronic kidney disease (CKD) arose from observations in kidney transplantation. APOL1 genotyping could soon improve the safety of living kidney donation in individuals with recent African ancestry and alter the allocation of deceased donor kidneys.

methodsThis article reviews the potential mechanisms that underlie development of APOL1-associated nephropathy. Roles for circulating APOL1 protein versus intrinsic renal expression of APOL1 are discussed, as well as the requirement for modifying genetic and/or environmental factors.

resultsAbundant evidence supports local kidney production of APOL1 renal-risk variant protein in the development of nephropathy; this is true in both native kidney disease and after renal transplantation. Only a minority of kidneys from individuals with APOL1 high-risk genotypes will develop CKD or manifest shorter renal allograft survival after transplantation. Therefore, modifying factors that explain why only a subset of kidneys develops nephropathy remain critical to identify. It appears likely that environmental exposures, as opposed to major APOL1-second gene interactions, will prove to be stronger modifiers of the risk for nephropathy.

conclusionsThe evolving understanding of the pathogenesis in APOL1-associated nephropathy will identify biomarkers predicting nephropathy in individuals at high genetic risk and lead to novel therapies to prevent or slow native CKD progression and prolong survival of transplanted kidneys. In the interim, the National Institutes of Health-sponsored "APOL1 Long-term Kidney Transplantation Outcomes" Network will determine whether APOL1 genotyping in individuals with recent African ancestry improves outcomes and safety in kidney transplantation.

Indexed as

AnimalsApolipoprotein L1Black or African AmericanDisease ProgressionGene-Environment InteractionGenotypeGraft SurvivalHumansKidneyKidney Failure, ChronicKidney TransplantationMiceMice, TransgenicPatient SafetyRenal InsufficiencyRenal Insufficiency, ChronicAPOL1 protein, humanApolipoprotein L1

Identifiers

PMID30371607
PMCPMC6226011
OpenAlexW2898783422

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.