Evidence map›Paper›PMID 30077216›Full record

ArticleMayo Clinic proceedings2018

C3 Glomerulopathy: Ten Years' Experience at Mayo Clinic.

Aishwarya Ravindran, Fernando C Fervenza, Richard J H Smith, An S De Vriese, Sanjeev Sethi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mayo Clinic proceedings, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
–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

75 citing papers in PubMed.

  1. Article
  2. Review
  3. [Immune complex- and complement-mediated glomerulonephritides].Innere Medizin (Heidelberg, Germany) · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Kidney international reports · 2025
    Article
  12. Guarding glomeruli from immune injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

15 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Aishwarya RavindranDivision of Anatomic Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN.
Fernando C FervenzaDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, MN.
Richard J H SmithMolecular Otolaryngology and Renal Research Laboratories, Division of Nephrology, Department of Internal Medicine, Carver College of Medicine, Iowa City, IA; Department of Pediatrics, Carver College of Medicine, Iowa City, IA.
An S De VrieseDivision of Nephrology, Department of Internal Medicine, AZ Sint-Jan Brugge-Oostende, Brugge, and Ghent University, Ghent, Belgium.
Sanjeev SethiDivision of Anatomic Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN. Electronic address: sethi.sanjeev@mayo.edu.

Funding

C3 Glomerulopathy -- A Collaborative StudyR01DK110023 · NIDDK · UNIVERSITY OF IOWA · PI Patrick Breheny, Carla M Nester · 2017 to 2026
$5.6M
NIDDK NIH HHS R01 DK110023
6 · The paper itself

Abstract

objectiveTo describe the clinicopathological features, complement abnormalities, triggers, treatment, and outcomes of C3 glomerulopathy. PATIENTS AND

methodsA total of 114 patients with C3 glomerulopathy seen at Mayo Clinic from January 1, 2007, through December 31, 2016, were evaluated in this study.

resultsThe mean age at diagnosis for the entire cohort was 40.4±22.3 years, with a median serum creatinine level and proteinuria value of 1.6 mg/dL (range: 0.3-14.7) (to convert to mmol/L, multiply by 0.0259) and 2605 mg/24 h (range: 233-24,165), respectively. Hematuria was present in 100 patients (87.7%). The C3 and C4 levels were low in 50 of 112 (44.6%) and 13 of 110 (11.8%) patients, respectively. A history of infection, positive autoimmune findings, and monoclonal gammopathy (MIg) were present in 33 of 114 (28.9%), 28 of 114 (24.6%), and 36 of 95 (37.9%) patients, respectively. However, 28 of 43 patients 50 years or older (65.1%) had MIg. A genetic variant in complement genes, C3 nephritic factor (C3Nef), and other autoantibodies was present in 26 of 70 (37.1%), 30 of 69 (43.5%), and 9 of 67 (13.4%) patients, respectively. Membranoproliferative and mesangial proliferative glomerulonephritis were the common patterns of injury. Patients without MIg were younger (mean age, 32.3±20.6 years), with a median serum creatinine level and proteinuria value of 1.4 mg/dL (range: 0.3-7.9) and 2450 mg/24 h (range: 250-24, 165) and with low C3 and C4 levels in 38 of 77 (49.4%) and 9 of 75 (12.0%) patients, respectively. Most patients received corticosteroids and other immunosuppressive drugs. In patients without MIg, at a median follow-up of 22.3 months (range: 0.1-201.1), the median serum creatinine level and proteinuria value were 1.4 mg/dL (range: 0.3-3.7) and 825.5 mg/24 h (range: 76-22, 603), and 7 patients (9.2%) had progression to end-stage renal disease.

conclusionC3 glomerulopathy is a heterogeneous disease entity with complex triggering events and abnormalities of the alternative pathway of complement. The disease tends to be progressive and exhibits a variable response to immunosuppressive therapy.

Indexed as

GlomerulonephritisAdolescentAdultAgedAged, 80 and overAutoantibodiesAutoimmune DiseasesChildChild, PreschoolComplement C3Complement C3 Nephritic FactorComplement Factor HComplement System ProteinsCreatinineDisease ProgressionFemaleAutoantibodiesC3 protein, humancomplement 4 nephritic factorComplement C3Complement C3 Nephritic FactorComplement Factor HComplement System ProteinsCreatinineGlucocorticoidsImmunoglobulinsImmunosuppressive Agents

Identifiers

PMID30077216
PMCPMC6312642

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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.