Evidence map›Paper›PMID 19838113›Full record

ReviewCurrent opinion in nephrology and hypertension2010

Susceptibility genes in common complex kidney disease.

Jasmin Divers, Barry I Freedman

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

12 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Chapter 8: Future directions and controversies.Kidney international supplements · 2012
    Article
  6. Review
  7. Genetics of kidney failure and the evolving story of APOL1.The Journal of clinical investigation · 2011
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Genetic kidney diseases.Lancet (London, England) · 2010
    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.

Jasmin DiversDivision of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1053, USA.
Barry I Freedman
Wake Forest University · US

Funding

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
GENETIC ANALYSIS OF HUMAN HYPERTENSIVE ESRDR01HL056266 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI FREEDMAN, BARRY IRA · 1997 to 2001
$466k
NHLBI NIH HHS R01 HL056266NIDDK NIH HHS R01 DK070941
6 · The paper itself

Abstract

purpose of reviewThis paper reviews recent efforts to identify genetic variants conferring risk for chronic kidney disease. A brief overview of methods for identifying gene variants is provided, along with genetic associations and new avenues under exploration. RECENT

findingsThe role of renal failure susceptibility genes, including MYH9, ELMO1, UMOD and ACTN4, has become clearer over the past 18 months. The spectrum of MYH9-associated kidney disease, including focal segmental glomerulosclerosis, global glomerulosclerosis and collapsing glomerulopathy, related entities contributing to approximately 43% of end-stage renal disease in African-Americans, has come to light. SUMMARY: MYH9 will re-categorize focal segmental glomerulosclerosis and related disorders, and has clarified the relationship between hypertension and kidney disease. MYH9 polymorphisms account for much of the excess risk of HIV-associated nephropathy and nondiabetic kidney disease in African-Americans. Kidney disease associations with ELMO1 and UMOD have been replicated and applications of genome-wide association studies based on expression data are providing novel insights on renal protein expression. These breakthroughs will alter our approach to kidney disease surveillance and lead to new therapeutic options.

Indexed as

ActininAdaptor Proteins, Signal TransducingAIDS-Associated NephropathyBlack or African AmericanChromosome MappingDiabetic NephropathiesGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansKidneyKidney DiseasesLinkage DisequilibriumMolecular Motor ProteinsMucoproteinsMyosin Heavy ChainsActininACTN4 protein, humanAdaptor Proteins, Signal TransducingELMO1 protein, humanMolecular Motor ProteinsMucoproteinsMYH9 protein, humanMyosin Heavy ChainsUMOD protein, humanUromodulin

Identifiers

PMID19838113
PMCPMC2883259
OpenAlexW2046310013

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.