Evidence map›Paper›PMID 40535909›Full record

ArticleKidney medicine2025

C3 Glomerulonephritis Associated With Unusual IgG4 Antifactor H in IgG4-related Disease.

Paul Dalmas, Mickael Bobot, Noémie Jourde-Chiche, Julie Bruno, Stéphane Burtey, Laurent Daniel, Carine El-Sissy, Véronique Fremeaux-Bacchi, Antonio Jorquera, Vincent Javaugue and 2 more

Abstract readCase Reports
In one paragraph

Article in Kidney medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Paul DalmasAix-Marseille Univ, APHM, hôpital de la Timone, Internal Medicine Department, Marseille, France.
Mickael BobotC2VN, INSERM, INRAE, Aix-Marseille Université, Marseille, France.
Noémie Jourde-ChicheC2VN, INSERM, INRAE, Aix-Marseille Université, Marseille, France.
Julie BrunoC2VN, INSERM, INRAE, Aix-Marseille Université, Marseille, France.
Stéphane BurteyC2VN, INSERM, INRAE, Aix-Marseille Université, Marseille, France.
Laurent DanielC2VN, INSERM, INRAE, Aix-Marseille Université, Marseille, France.
Carine El-SissyDepartment of Immunology, AP-HP, Georges Pompidou European Hospital, Paris, France.
Véronique Fremeaux-BacchiDepartment of Immunology, AP-HP, Georges Pompidou European Hospital, Paris, France.
Antonio JorqueraDepartment of Pathology and Ultrastructural Pathology, Centre Hospitalier Universitaire, Poitiers, France.
Vincent JavaugueControl of the immune response B and lymphoproliferation, CNRS UMR 7276, INSERM UMR 1262, University of Limoges, Centre de référence de l'amylose AL et autres maladies par dépôts d'immunoglobuline monoclonale, Limoges, France.
Nicolas SchleinitzAix-Marseille Univ, APHM, hôpital de la Timone, Internal Medicine Department, Marseille, France.
Mikael EbboAix-Marseille Univ, APHM, hôpital de la Timone, Internal Medicine Department, Marseille, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C3 glomerulonephritis (C3GN) is characterized by glomerular aggression mediated by deregulation of the alternative complement pathway. C3GN can be inherited or consequent to acquired autoantibodies, notably against factor H. We report the case of a patient with systemic active IgG4-related disease who presented for acute kidney injury with glomerular proteinuria and hypocomplementemia related to C3GN associated with IgG4-related interstitial nephritis on kidney biopsy. Factor H was low, and antifactor H IgG autoantibody was detected. Detection of other acquired or genetic complement alternative pathway disorders returned negative. After initial failure of oral corticoids and intravenous rituximab, the patient was successfully treated by intravenous cyclophosphamide followed by maintenance therapy with rituximab. Antifactor H autoantibody isotypes were IgG1 and IgG3, mainly as all antifactor H in positive controls but also IgG4, which is unusual. This suggests a link in this case between the oligoclonal expansion of plasma cells in IgG4-related disease and the production of antifactor H antibodies, especially of IgG4 isotype.

Indexed as

Antifactor HC3 glomerulonephritisIgG4-related disease

Identifiers

PMID40535909
PMCPMC12173104

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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.