Evidence map›Paper›PMID 35734939›Full record

ReviewAmerican journal of medical genetics. Part C, Seminars in medical genetics2022

C3 glomerulopathy: Understanding an ultra-rare complement-mediated renal disease.

Amanda K Heiderscheit, Jill J Hauer, Richard J H Smith

Open access · hybridAbstract readReview
In one paragraph

Review in American journal of medical genetics. Part C, Seminars in medical genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Time to move to a cluster-based management of C3G/IC-MPGN.Pediatric nephrology (Berlin, Germany) · 2026
    Article
  5. Article
  6. Review
  7. Proteomic Profiling of Complement Components in Glomerular Disease.Laboratory investigation; a journal of technical methods and pathology · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. A Narrative Review of C3 Glomerulopathy: From Pathogenesis to Targeted Therapy.Canadian journal of kidney health and disease · 2026
    Review
  12. Review
  13. Review
  14. Article
  15. Complement System Inhibitors in Nephrology: An Update-Narrative Review.International journal of molecular sciences · 2025
    Review
  16. Review
  17. Evaluation for genetic disease in kidney transplant candidates: A practice resource.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025
    Review
  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

3 authors at 1 institution in 1 country.

Amanda K HeiderscheitMolecular Otolaryngology and Renal Research Laboratories, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA.ORCID 0000-0003-0223-7274
Jill J HauerMolecular Otolaryngology and Renal Research Laboratories, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA.ORCID 0000-0003-3455-6536
Richard J H SmithMolecular Otolaryngology and Renal Research Laboratories, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA.
University of Iowa · US

Funding

C3 Glomerulopathy -- A Collaborative StudyR01DK110023 · NIDDK · UNIVERSITY OF IOWA · PI Patrick Breheny, Carla M Nester · 2017 to 2026
$5.6M
Blood Cells in Hemostasis and ThrombosisT32HL086344 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GINSBERG, MARK HOWARD · 2008 to 2023
$4.4M
NHLBI NIH HHS T32 HL086344NIDDK NIH HHS R01 DK110023
6 · The paper itself

Abstract

C3 glomerulopathy (C3G) describes a pathologic pattern of injury diagnosed by renal biopsy. It is characterized by the dominant deposition of the third component of complement (C3) in the renal glomerulus as resolved by immunofluorescence microscopy. The underlying pathophysiology is driven by dysregulation of the alternative pathway of complement in the fluid-phase and in the glomerular microenvironment. Characterization of clinical features and a targeted evaluation for indices and drivers of complement dysregulation are necessary for optimal patient care. Autoantibodies to the C3 and C5 convertases of complement are the most commonly detected drivers of complement dysregulation, although genetic mutations in complement genes can also be found. Approximately half of patients progress to end-stage renal disease within 10 years of diagnosis, and, while transplantation is a viable option, there is high risk for disease recurrence and allograft failure. This poor outcome reflects the lack of disease-specific therapy for C3G, relegating patients to symptomatic treatment to minimize proteinuria and suppress renal inflammation. Fortunately, the future is bright as several anti-complement drugs are currently in clinical trials.

Indexed as

Glomerulonephritis, MembranoproliferativeKidney DiseasesHumansKidneyRare DiseasesC3 glomerulonephritisC3 glomerulopathydense deposit disease

Identifiers

PMID35734939
PMCPMC9613507
OpenAlexW4283312476

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.