Evidence map›Paper›PMID 21881214›Full record

ReviewThe Journal of clinical investigation2011

Genetics of kidney failure and the evolving story of APOL1.

David J Friedman, Martin R Pollak

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Guideline
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  16. Antisense oligonucleotides ameliorate kidney dysfunction in podocyte-specific APOL1 risk variant mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
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  18. Review
  19. Article
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15 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

David J FriedmanNephrology Division, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA. dfriedma@bidmc.harvard.edu
Martin R Pollak
Beth Israel Deaconess Medical Center · USBroad Institute · US

Funding

The Genetic Basis of FSGSR01DK054931 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI POLLAK, MARTIN R. · 1999 to 2017
$6.2M
NIDDK NIH HHS R01 DK054931
6 · The paper itself

Abstract

Chronic kidney disease (CKD) results from a wide array of processes that impair the kidney's ability to perform its major functions. As many as 20 million Americans suffer from CKD and nearly a half million from end-stage renal disease, but there are also examples of centenarians with adequate renal function. Family-based and genome-wide studies suggest that genetic differences substantially influence an individual's lifetime risk for kidney disease. One emerging theme is that evolution of genes related to host defense against pathogens may limit kidney longevity. The identification of these genetic factors will be critical for expanding our understanding of renal development and function as well as for the design of novel therapeutics for kidney disease.

Indexed as

Biological EvolutionApolipoprotein L1ApolipoproteinsGene FrequencyGenetic Predisposition to DiseaseGenetic VariationGenome, HumanHumansKidney DiseasesLipoproteins, HDLPhenotypeRenal InsufficiencyRenal Insufficiency, ChronicRisk FactorsAPOL1 protein, humanApolipoprotein L1ApolipoproteinsLipoproteins, HDL

Identifiers

PMID21881214
PMCPMC3163957
OpenAlexW2084067015

What OpenQuestion holds

Textmetadata
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.