Evidence map›Paper›PMID 21455721›Full record

ReviewPediatric nephrology (Berlin, Germany)2012

Glomerular pathology in Alport syndrome: a molecular perspective.

Dominic Cosgrove

Abstract readReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 41 citations in OpenAlex.

  1. Pathological diagnosis of Alport syndrome.Kidney research and clinical practice · 2025
    Article
  2. Review
  3. The extracellular matrix complexity of idiopathic epiretinal membranes and the bilaminar arrangement of the associated internal limiting membrane in the posterior retina.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2021
    Article
  4. Review
  5. Article
  6. Review
  7. Podocyte p53 Limits the Severity of Experimental Alport Syndrome.Journal of the American Society of Nephrology : JASN · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. 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

1 author at 1 institution in 1 country.

Dominic CosgroveBoys Town National Research Hospital, Omaha, NE 68131, USA. cosgrove@boystown.org
Boys Town · US

Funding

MOLECULAR ASPECTS OF ALPORT RENAL DISEASE PROGRESSIONR01DK055000 · NIDDK · FATHER FLANAGAN'S BOYS'HOME · PI COSGROVE, DOMINIC E. · 1999 to 2013
$3.0M
Matrix OtopathologyR01DC006442 · NIDCD · UNIVERSITY OF PENNSYLVANIA · PI GRATTON, MICHAEL ANNE NMI · 2004 to 2011
$2.6M
NIDCD NIH HHS R01 DC006442NIDDK NIH HHS R01 DK055000
6 · The paper itself

Abstract

We have known for some time that mutations in the genes encoding 3 of the 6 type IV collagen chains are the underlying defect responsible for both X-linked (where the COL4A5 gene is involved) and autosomal (where either COL4A3 or COL4A4 genes are involved) Alport syndrome. The result of these mutations is the absence of the sub-epithelial network of all three chains in the glomerular basement membrane (GBM), resulting, at maturity, in a type IV collagen GBM network comprising only α1(IV) and α2(IV) chains. The altered GBM functions adequately in early life. Eventually, there is onset of proteinuria associated with the classic and progressive irregular thickening, thinning, and splitting of the GBM, which culminates in end-stage renal failure. We have learned much about the molecular events associated with disease onset and progression through the study of animal models for Alport syndrome, and have identified some potential therapeutic approaches that may serve to delay the onset or slow the progression of the disease. This review focuses on where we are in our understanding of the disease, where we need to go to understand the molecular triggers that set the process in motion, and what emergent therapeutic approaches show promise for ameliorating disease progression in the clinic.

Indexed as

AnimalsCollagen Type IVDisease ProgressionGenetic Predisposition to DiseaseHumansKidney Failure, ChronicKidney GlomerulusModels, AnimalMutationNephritis, HereditaryPhenotypePrognosisProteinuriaCollagen Type IV

Identifiers

PMID21455721
PMCPMC3484979
OpenAlexW1987964936

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.