Evidence map›Paper›PMID 27056062›Full record

ReviewPediatric nephrology (Berlin, Germany)2017

C3 Glomerulopathy.

Magdalena Riedl, Paul Thorner, Christoph Licht

Abstract readReview
PubMed Publisher
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 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
–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

42 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Meningococcal Vaccination: Recommendations of the Advisory Committee on Immunization Practices, United States, 2020.MMWR. Recommendations and reports : Morbidity and mortality weekly report. Recommendations and reports · 2020
    Guideline
  2. Trial
  3. Article
  4. A Narrative Review of C3 Glomerulopathy: From Pathogenesis to Targeted Therapy.Canadian journal of kidney health and disease · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Low C3 in a 4-month-old baby: is it a problem?Pediatric nephrology (Berlin, Germany) · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Adjustment ofFrontiers in genetics · 2023
    Article
  16. Article
  17. Novel Insights into Factor D Inhibition.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Article
  20. A rare cause of postinfectious glomerulonephritis: Answers.Pediatric nephrology (Berlin, Germany) · 2021
    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

3 authors.

Magdalena RiedlCell Biology Program of the Research Institute, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada.
Paul ThornerDepartment of Pediatric Laboratory Medicine, The Hospital for Sick Children, Toronto, ON, Canada.
Christoph LichtCell Biology Program of the Research Institute, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada. christoph.licht@sickkids.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent advances in our understanding of the disease pathology of membranoproliferative glomerulonephritis has resulted in its re-classification as complement C3 glomerulopathy (C3G) and immune complex-mediated glomerulonephritis (IC-GN). The new consensus is based on its underlying pathomechanism, with a key pathogenetic role for the complement alternative pathway (AP), rather than on histomorphological characteristics. In C3G, loss of AP regulation leads to predominant glomerular C3 deposition, which distinguishes C3G from IC-GN with predominant immunoglobulin G staining. Electron microscopy further subdivides C3G into C3 glomerulonephritis and dense deposit disease depending on the presence and distribution pattern of electron-dense deposits within the glomerular filter. Mutations or autoantibodies affecting the function of AP activators or regulators, in particular the decay of the C3 convertase (C3 nephritic factor), have been detected in up to 80 % of C3G patients. The natural outcome of C3G is heterogeneous, but 50 % of patients progress slowly and reach end-stage renal disease within 10-15 years. The new classification not only marks significant advancement in the pathogenic understanding of this rare disease, but also opens doors towards more specific treatment with the potential for improved outcomes.

Indexed as

Complement C3AnimalsComplement C3 Nephritic FactorDisease Models, AnimalGlomerulonephritis, MembranoproliferativeHumansTreatment OutcomeC3 protein, humanComplement C3Complement C3 Nephritic FactorC3 GlomerulopathyC3 Nephritic factorComplementDense deposit diseaseEculizumabMembranoproliferative glomerulonephritis

Identifiers

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.