ArticleKidney international2012
Sensitive and specific assays for C3 nephritic factors clarify mechanisms underlying complement dysregulation.
Article in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 99 citations in OpenAlex.
- Clinical improvement of acquired partial lipodystrophy in an adolescent with C3 glomerulopathy treated with pegcetacoplan.Pediatric nephrology (Berlin, Germany) · 2026Article
- Characterizing Properdin-Inhibited C3 Nephritic Factors in Patients with Complement-Mediated Kidney Diseases.International journal of molecular sciences · 2026Article
- Canadian Society of Nephrology Commentary on the Evolving Kidney Disease Improving Global Outcomes Adult Glomerulonephritis Guidelines.Canadian journal of kidney health and disease · 2026Article
- IdeZ protease does not prevent convertase stabilization by C3 nephritic factors in C3 glomerulopathy.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Article
- Acquired drivers of C3 glomerulopathy.Clinical kidney journal · 2025Review
- Functional Characterization of Anti-C3bBb Autoantibodies and C3 Glomerulopathy Phenotype.Journal of the American Society of Nephrology : JASN · 2025Article
- Improved therapeutic efficacy of a bifunctional anti-C5 mAb-FH SCR1-5 fusion protein over anti-C5 mAb in an accelerated mouse model of C3 glomerulopathy.ImmunoHorizons · 2025Article
- A Cell-Based Assay to Measure the Activity of the Complement Convertases.Kidney international reports · 2024Article
- Evaluation of the significance of complement-related genes mutations in atypical postinfectious glomerulonephritis: a pilot study.International urology and nephrology · 2024Article
- Defining Nephritic Factors as Diverse Drivers of Systemic Complement Dysregulation in C3 Glomerulopathy.Kidney international reports · 2024Article
- Complements and Their Role in Systemic Disorders.Cureus · 2024Review
- A Nef Precursor or Benign Counterpart: High Prevalence of Healthy Subjects with Antibody Reactivity to the C3-Convertase.Kidney360 · 2023Article
- A Monoclonal Antibody That Provides a Model for C3 Nephritic Factors.Monoclonal antibodies in immunodiagnosis and immunotherapy · 2023Article
- Kidney diseases.Immunological reviews · 2023Review
- C3 glomerulopathies: dense deposit disease and C3 glomerulonephritis.Frontiers in medicine · 2023Review
- Immunoelectron microscopy findings in a patient with C3 glomerulonephritis.Clinical nephrology. Case studies · 2023Article
- Gross hematuria, edema, and hypocomplementemia in a 9-year-old boy: Answers.Pediatric nephrology (Berlin, Germany) · 2022Article
- A case of C3 glomerulopathy with nephritis-associated plasmin receptor positivity without a history of streptococcal infection.CEN case reports · 2022Article
- Challenges in diagnostic testing of nephritic factors.Frontiers in immunology · 2022Review
- Autoantibodies Against the Complement Regulator Factor H in the Serum of Patients With Neuromyelitis Optica Spectrum Disorder.Frontiers in immunology · 2021Article
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Authors and funding
9 authors at 6 institutions in 4 countries.
Funding
Abstract
C3 nephritic factors are autoantibodies that prolong the half-life or prevent regulation of the alternative pathway C3 convertase, resulting in uncontrolled complement activation. They are strongly associated with renal disease but their role in pathogenesis remains controversial. Here we optimized and compared a panel of assays to identify and interrogate nephritic factor activities. Of 101 patients with histologic or clinically evident disease, 48 were positive in some or all assays. In the presence of properdin, binding of autoantibody was detected in 39 samples and convertase stabilization was detected in 36. Forty-two of 48 nephritic factors tested prevented convertase decay by factor H, and most of these by decay accelerating factor (28) and complement receptor 1 (34). Representative properdin-independent nephritic factors had no effect on C5 cleavage and terminal pathway activity, while properdin-dependent nephritic factors enhanced activity. Biacore analysis of four purified IgG samples confirmed resistance to decay and showed that properdin-independent nephritic factors increased convertase half-life over 50-fold, whereas properdin-dependent nephritic factors increased the half-life 10- to 20-fold and also increased activity of the C3 convertase up to 10-fold. Thus, our study provides a rational approach to detect and characterize nephritic factors in patients.
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