Evidence map›Paper›PMID 22903660›Full record

ReviewPediatric nephrology (Berlin, Germany)2013

An update on the pathomechanisms and future therapies of Alport syndrome.

Damien Noone, Christoph Licht

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. NRF2 Dysregulation and Therapeutic Insights Across Chronic Kidney Diseases.International journal of molecular sciences · 2025
    Review
  6. Genotype-Based Molecular Mechanisms in Alport Syndrome.Journal of the American Society of Nephrology : JASN · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Childhood risk factors for adulthood chronic kidney disease.Pediatric nephrology (Berlin, Germany) · 2021
    Review
  11. Article
  12. Article
  13. Neonatal stroke and haematuria: Answers.Pediatric nephrology (Berlin, Germany) · 2018
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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 1 institution in 1 country.

Damien NooneDivision of Nephrology, Department of Paediatrics, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada.
Christoph Licht
Hospital for Sick Children · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alport Syndrome (AS) is an inherited progressive disease that is caused by mutations of the genes encoding the key collagen chains, α3, α4, and α5, which are necessary for the composition of collagen type IV to form a robust glomerular basement membrane (GBM), capable of withstanding the significant biomechanical strain to which the glomerulus is subjected. Progressive loss of the filtration barrier allows excessive proteinuria, which ultimately leads to end-stage kidney disease (ESKD). The evidence for a beneficial renoprotective effect of renin-angiotensin-aldosterone system (RAAS) blockade by angiotensin-converting enzyme (ACE) inhibition and/or angiotensin receptor blockers (ARBs) is well established in AS and recent evidence has shown that it can significantly delay the time to onset of renal replacement therapy and ESKD. Future potential treatments of AS disease progression are evaluated in this review.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAngiotensin II Type 1 Receptor BlockersAnimalsCollagen Type IVDisease ProgressionFibrosisGenetic Predisposition to DiseaseHumansKidneyKidney Failure, ChronicMutationNephritis, HereditaryPhenotypeProteinuriaRenal AgentsRenin-Angiotensin SystemAngiotensin-Converting Enzyme InhibitorsAngiotensin II Type 1 Receptor BlockersCollagen Type IVRenal Agents

Identifiers

PMID22903660
OpenAlexW2028670169

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.