Evidence map›Paper›PMID 27470160›Full record

ReviewPediatric nephrology (Berlin, Germany)2017

Genetics of childhood steroid-sensitive nephrotic syndrome.

Alana M Karp, Rasheed A Gbadegesin

Open access · greenAbstract readReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.4field-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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Treatment of steroid-resistant nephrotic syndrome in the genomic era.Pediatric nephrology (Berlin, Germany) · 2019
    Review
  11. Observational
  12. Observational
  13. Article
  14. Article
  15. Review
  16. Genetic Basis of Health Disparity in Childhood Nephrotic Syndrome.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2018
    Review
  17. Review
  18. Observational
  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

2 authors at 2 institutions in 1 country.

Alana M KarpDepartment of Pediatrics, Division of Nephrology, Emory University, Atlanta, GA, USA.
Rasheed A GbadegesinDepartment of Pediatrics, Division of Nephrology, Duke University Medical Center, Durham, NC, USA. rasheed.gbadegesin@duke.edu.
Duke Medical Center · USEmory University · US

Funding

Gene Discovery in Autosomal Dominant Focal Segmental GlomerulosclerosisR01DK094987 · NIDDK · DUKE UNIVERSITY · PI GBADEGESIN, RASHEED ADEBAYO · 2012 to 2016
$2.5M
Functional and Phenotypic Characterization of a New FSGS GeneR01DK098135 · NIDDK · DUKE UNIVERSITY · PI GBADEGESIN, RASHEED ADEBAYO · 2014 to 2018
$1.8M
Data commons for 'omic, microscopy and analysis core facilitiesS10OD018164 · OD · DUKE UNIVERSITY · PI WRAY, GREGORY A. · 2014 to 2014
$598k
Functional and Phenotypic Characterization of a New FSGS GeneR56DK098135 · NIDDK · DUKE UNIVERSITY · PI GBADEGESIN, RASHEED ADEBAYO · 2013 to 2013
$118k
NIDDK NIH HHS R01 DK094987NIDDK NIH HHS R01 DK098135NIDDK NIH HHS R56 DK098135NIH HHS S10 OD018164
6 · The paper itself

Abstract

The pathogenesis of childhood-onset nephrotic syndrome (NS), disparity in incidence of NS among races, and variable responses to therapies in children with NS have defied explanation to date. In the last 20 years over 50 genetic causes of steroid-resistant nephrotic syndrome (SRNS) have been identified, and at least two disease loci for two pathologic variants of SRNS (focal segmental glomerulosclerosis and membranous nephropathy) have been defined. However, the genetic causes and risk loci for steroid-sensitive nephrotic syndrome (SSNS) remain elusive, partly because SSNS is relatively rare and also because cases of SSNS vary widely in phenotypic expression over time. A recent study of a well-defined modest cohort of children with SSNS identified variants in HLA-DQA1 as a risk factor for SSNS. Here we review what is currently known about the genetics of SSNS and also discuss how recent careful phenotypic and genomic studies reinforce the role of adaptive immunity in the molecular mechanisms of SSNS.

Indexed as

Genetic LociAdaptive ImmunityChildDrug ResistanceGenetic Predisposition to DiseaseGlucocorticoidsHLA-DQ alpha-ChainsHumansIncidenceNephrotic SyndromeTreatment OutcomeGlucocorticoidsHLA-DQA1 antigenHLA-DQ alpha-ChainsGenetic risksGenomicsGWASNephrotic syndrome children

Identifiers

PMID27470160
PMCPMC5276801
OpenAlexW2479276026

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.