ArticleOrphanet journal of rare diseases2019
C4 nephritic factor in patients with immune-complex-mediated membranoproliferative glomerulonephritis and C3-glomerulopathy.
Article in Orphanet journal of rare diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Complement-Mediated Kidney Diseases: Role of Alternative Pathway in Glomerular Inflammation.Kidney international reports · 2026Review
- Primary membranoproliferative glomerulonephritis: natural history, pathogenesis, and treatment.Frontiers in nephrology · 2026Review
- Expert Discussion on Immune Complex-Mediated Membranoproliferative Glomerulonephritis: Challenges and Considerations.Advances in therapy · 2025Article
- Autoantibodies Against Factor B and Factor H Without Pathogenic Effects in a Patient with Immune Complex-Mediated Membranoproliferative Glomerulonephritis.Biomedicines · 2025Article
- Acquired drivers of C3 glomerulopathy.Clinical kidney journal · 2025Review
- Challenges in the Diagnosis and Management of Immune Complex-Mediated Membranoproliferative Glomerulonephritis and Complement 3 Glomerulopathy.Kidney international reports · 2025Review
- Defining Nephritic Factors as Diverse Drivers of Systemic Complement Dysregulation in C3 Glomerulopathy.Kidney international reports · 2024Article
- A clinical approach to children with C3 glomerulopathy.Pediatric nephrology (Berlin, Germany) · 2022Review
- Challenges in diagnostic testing of nephritic factors.Frontiers in immunology · 2022Review
- FHR-5 Serum Levels andFrontiers in immunology · 2021Article
- Different Aspects of Classical Pathway Overactivation in Patients With C3 Glomerulopathy and Immune Complex-Mediated Membranoproliferative Glomerulonephritis.Frontiers in immunology · 2021Article
- Complement C4, Infections, and Autoimmune Diseases.Frontiers in immunology · 2021Review
- Article
- Article
- C3 Glomerulopathy: A Current Perspective in an Evolving Landscape.Glomerular diseasesReview
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Authors and funding
61 authors at 20 institutions in 11 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcquired or genetic abnormalities of the complement alternative pathway are the primary cause of C3glomerulopathy(C3G) but may occur in immune-complex-mediated membranoproliferative glomerulonephritis (IC-MPGN) as well. Less is known about the presence and role of C4nephritic factor(C4NeF) which may stabilize the classical pathway C3-convertase. Our aim was to examine the presence of C4NeF and its connection with clinical features and with other pathogenic factors.
resultsOne hunfe IC-MPGN/C3G patients were enrolled in the study. C4NeF activity was determined by hemolytic assay utilizing sensitized sheep erythrocytes. Seventeen patients were positive for C4NeF with lower prevalence of renal impairment and lower C4d level, and higher C3 nephritic factor (C3NeF) prevalence at time of diagnosis compared to C4NeF negative patients. Patients positive for both C3NeF and C4NeF had the lowest C3 levels and highest terminal pathway activation. End-stage renal disease did not develop in any of the C4NeF positive patients during follow-up period. Positivity to other complement autoantibodies (anti-C1q, anti-C3) was also linked to the presence of nephritic factors. Unsupervised, data-driven cluster analysis identified a group of patients with high prevalence of multiple complement autoantibodies, including C4NeF.
conclusionsIn conclusion, C4NeF may be a possible cause of complement dysregulation in approximately 10-15% of IC-MPGN/C3G patients.
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