Evidence map›Paper›PMID 25810439›Full record

ReviewAmerican journal of physiology. Renal physiology2015

Translating genetic findings in hereditary nephrotic syndrome: the missing loops.

Gentzon Hall, Rasheed A Gbadegesin

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. CRB2 depletion induces YAP signaling and disrupts mechanosensing in podocytes.American journal of physiology. Renal physiology · 2025
    Article
  3. Review
  4. Review
  5. Treatment of steroid-resistant nephrotic syndrome in the genomic era.Pediatric nephrology (Berlin, Germany) · 2019
    Review
  6. Article
  7. Diagnostic and Management Challenges in Congenital Nephrotic Syndrome.Pediatric health, medicine and therapeutics · 2019
    Review
  8. Review
  9. The Human FSGS-CausingJournal of the American Society of Nephrology : JASN · 2018
    Article
  10. Article
  11. Article
  12. Urinary Anomalies in 22q11.2 Deletion (DiGeorge syndrome): From Copy Number Variations to Single-Gene Determinants of Phenotype.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2017
    Article
  13. Article
  14. 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.

Gentzon HallDepartment of Medicine and Duke Molecular Physiology Institute, Duke University Medical Center, Durham, North Carolina; and.
Rasheed A GbadegesinDepartment of Pediatrics and Duke Molecular Physiology Institute, Duke University Medical Center, Durham, North Carolina rasheed.gbadegesin@duke.edu.
Duke Medical Center · US

Funding

DUKE TRAINING GRANT IN NEPHROLOGYT32DK007731 · NIDDK · DUKE UNIVERSITY · PI CROWLEY, STEVEN D · 1995 to 2021
$3.6M
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
The Role of Interleukin-15 Receptor-alpha Variants in the Pathogenesis of FSGSK08DK111940 · NIDDK · DUKE UNIVERSITY · PI HALL, GENTZON · 2017 to 2021
$794k
Functional and Phenotypic Characterization of a New FSGS GeneR56DK098135 · NIDDK · DUKE UNIVERSITY · PI GBADEGESIN, RASHEED ADEBAYO · 2013 to 2013
$118k
NIDDK NIH HHS 5T32DK0007731NIDDK NIH HHS DK094987NIDDK NIH HHS DK098135-01A1NIDDK NIH HHS R01 DK094987NIDDK NIH HHS R01 DK098135
6 · The paper itself

Abstract

Nephrotic syndrome (NS) is a clinicopathological entity characterized by proteinuria, hypoalbuminemia, peripheral edema, and hyperlipidemia. It is the most common cause of glomerular disease in children and adults. Although the molecular pathogenesis of NS is not completely understood, data from the study of familial NS suggest that it is a "podocytopathy." Virtually all of the genes mutated in hereditary NS localize to the podocyte or its secreted products and the slit diaphragm. Since the completion of human genome sequence and the advent of next generation sequencing, at least 29 causes of single-gene NS have been identified. However, these findings have not been matched by therapeutic advances owing to suboptimal in vitro and in vivo models for the study of human glomerular disease and podocyte injury phenotypes. Multidisciplinary collaboration between clinicians, geneticists, cell biologists, and molecular physiologists has the potential to overcome this barrier and thereby speed up the translation of genetic findings into improved patient care.

Indexed as

HumansNephrotic SyndromePodocytesTranslational Research, Biomedicalgene mutationnephrotic syndromepodocyte

Identifiers

PMID25810439
PMCPMC4490379
OpenAlexW2030950567

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.