Evidence map›Paper›PMID 21712849›Full record

ReviewNature reviews. Nephrology2011

The genetics of common kidney disease: a pathway toward clinical relevance.

Paul E Drawz, John R Sedor

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Review
  2. Genome-Wide Analysis Studies and Chronic Kidney Disease.Kidney diseases (Basel, Switzerland) · 2017
    Review
  3. Review
  4. Integrative Biology of Diabetic Kidney Disease.Kidney diseases (Basel, Switzerland) · 2015
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Non-muscle myosins and the podocyte.Clinical kidney journal · 2012
    Article
  10. Genetic risk prediction for CKD: a journey of a thousand miles.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2012
    Article
  11. 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.

Paul E DrawzCenter for Study of Kidney Disease and Biology, 2500 MetroHealth Drive R415, Cleveland, OH 44109-1998, USA.
John R Sedor

Funding

CWRU NEPHROLOGY TRAINING PROGRAMT32DK007470 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SEDOR, JOHN R. · 1986 to 2019
$2.9M
GENETIC REGULATION OF RENAL DISEASE PROGRESSIONU01DK057329 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SEDOR, JOHN R. · 1999 to 2006
$2.3M
NIDDK NIH HHS T32 DK007470NIDDK NIH HHS U01 DK057329
6 · The paper itself

Abstract

Genome-wide association studies (GWASs) have advanced our understanding of the genetic basis for common renal diseases, including chronic kidney disease (CKD) and related traits such as hypertension. The 'common variant, common disease' hypothesis-the theoretical basis for gene mapping by GWASs-has, however, underestimated the complexity of the genetic architecture underlying these diseases. The disease-specific variants identified by GWASs, despite being supported by statistically robust associations, often fail to illuminate the biology underlying the association and explain only a small portion of the estimated heritability of these diseases, even in aggregate. Although these variants have highlighted novel pathways that can be targeted therapeutically, their small effect sizes have minimal effects on diagnosis, prognosis, and management of individual patients. At present, therefore, the data do not support the routine use of genetic testing in the management of patients with CKD. Advances in technology, such as massively parallel gene sequencing, and characterization of alternative modes of inheritance should further elucidate the genetic architecture of CKD and provide tools to improve patient care.

Indexed as

Apolipoprotein L1ApolipoproteinsGenetic MarkersGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansKidney DiseasesLipoproteins, HDLModels, GeneticMolecular Motor ProteinsMyosin Heavy ChainsPharmacogeneticsRisk AssessmentAPOL1 protein, humanApolipoprotein L1ApolipoproteinsGenetic MarkersLipoproteins, HDLMolecular Motor ProteinsMYH9 protein, humanMyosin Heavy Chains

Identifiers

PMID21712849

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.