Evidence map›Paper›PMID 36751667›Full record

ReviewGlomerular diseases2022

C3 Glomerulopathy: A Review with Emphasis on Ultrastructural Features.

Jean Hou, Kevin Yi Mi Ren, Mark Haas

Open access · goldAbstract readReview
In one paragraph

Review in Glomerular diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  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. Review
  7. Article
  8. Acquired drivers of C3 glomerulopathy.Clinical kidney journal · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. 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

3 authors at 2 institutions in 2 countries.

Jean HouDepartment of Pathology and Laboratory Medicine, Cedars Sinai Medical Center, Los Angeles, California, USA.
Kevin Yi Mi RenDepartment of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Mark HaasDepartment of Pathology and Laboratory Medicine, Cedars Sinai Medical Center, Los Angeles, California, USA.
Cedars-Sinai Medical Center · USQueen's University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C3 glomerulopathy (C3G) is a rare disease resulting from dysregulation of the alternative complement pathway, resulting in the deposition of complement component 3 (C3) in the kidney. It encompasses two major subgroups: dense deposit disease and C3 glomerulonephritis (C3GN). Although the alternative complement pathway is typically a very tightly controlled system, dysregulation can be a result of genetic mutations in the fluid phase or membrane-bound inhibitors or accelerators. In addition, de novo/acquired autoantibodies against any of the regulatory proteins can alter complement activation either by negating an inhibitor or activating an accelerator. Triggering events can be complex; however, the final pathway is characterized by the uncontrolled deposition of C3 in glomeruli and the formation of the membrane attack complex. Light microscopic findings can be quite heterogeneous with a membranoproliferative pattern most commonly encountered. Diagnostic confirmation of C3G is based on a characteristic pattern of glomerular immunofluorescence staining, with C3-dominant deposits that are at least 2 orders of intensity greater than staining for any immunoglobulin (Ig) or C1q. Electron microscopy is necessary for diagnosing DDD in particular, but can also help to distinguish C3GN from other glomerular disease mimickers.

Indexed as

C3 glomerulopathyElectron microscopyRenal pathologyUltrastructural pathology

Identifiers

PMID36751667
PMCPMC9710331
OpenAlexW4223450638

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.