Evidence map›Paper›PMID 24233469›Full record

ReviewClinical and experimental nephrology2014

The biology of APOL1 with insights into the association between APOL1 variants and chronic kidney disease.

Sethu M Madhavan, John F O'Toole

Abstract readReview
In one paragraph

Review in Clinical and experimental nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. A focus on the association of Apol1 with kidney disease in children.Pediatric nephrology (Berlin, Germany) · 2021
    Review
  7. 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 at 1 institution in 1 country.

Sethu M Madhavan
John F O'Toole
Case Western Reserve University · US

Funding

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
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
NIDDK NIH HHS R01 DK097836NIDDK NIH HHS R56 DK097836
6 · The paper itself

Abstract

Recent studies have identified genetic variants in APOL1 that may contribute to the increased incidence of kidney disease in populations with African ancestry. Here, we review the biology of APOL1 present in the circulation and localized to the kidney as it may contribute to the pathogenesis of APOL1-associated kidney disease.

Indexed as

Apolipoprotein L1ApolipoproteinsBlack PeopleGenetic VariationHumansLipoproteins, HDLPolymorphism, Single NucleotideRenal Insufficiency, ChronicTrypanosoma brucei gambienseTrypanosomiasis, AfricanAPOL1 protein, humanApolipoprotein L1ApolipoproteinsLipoproteins, HDL

Identifiers

PMID24233469
PMCPMC4022720
OpenAlexW1974845434

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.