ArticleKidney international reports2024
Defining Nephritic Factors as Diverse Drivers of Systemic Complement Dysregulation in C3 Glomerulopathy.
Article in Kidney international reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Characterizing Properdin-Inhibited C3 Nephritic Factors in Patients with Complement-Mediated Kidney Diseases.International journal of molecular sciences · 2026Article
- Biomarkers in the Management of Complement-Mediated Kidney Diseases in the Era of Complement Therapeutics.Clinical journal of the American Society of Nephrology : CJASN · 2026Review
- C3 glomerulopathy in transplant "like yet unlike native": Pathophysiology, recent advances in therapeutics and evolving paradigms.World journal of transplantation · 2026Review
- Complement Dysregulation in Kidney Diseases: Mechanisms, Biomarkers, and Emerging Targeted Therapies.International journal of molecular sciences · 2026Review
- Recurrence of C3 Glomerulopathy and Immune Complex-Mediated Membranoproliferative Glomerulonephritis After Kidney Transplantation: Challenges and Opportunities.Kidney international reports · 2026Review
- Article
- Complement diagnostics and therapeutics for the pediatric population: early successes and opportunities for further advancement.Frontiers in pharmacology · 2026Review
- From immune dysregulation to renal injury: mechanistic insights and translational opportunities in immune-mediated nephropathies.Frontiers in cell and developmental biology · 2026Review
- Current and Emerging Therapies for C3 Glomerulopathy and Primary (Idiopathic) Immune Complex Membranoproliferative Glomerulonephritis.Kidney international reports · 2026Review
- Kidney transplant in patients with C3 glomerulopathy.Clinical kidney journal · 2025Review
- 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
- Functional Characterization of Anti-C3bBb Autoantibodies and C3 Glomerulopathy Phenotype.Journal of the American Society of Nephrology : JASN · 2025Article
- Factor H-related 1 and heparan sulfate architecture contribute to complement dysregulation in C3 glomerulopathy.Frontiers in immunology · 2025Article
- Establishing the Future Direction of Clinical Outcomes in C3 Glomerulopathy: Perspectives From a Patient and a Physician.Kidney medicine · 2025Review
- C3 Glomerulopathy: A Current Perspective in an Evolving Landscape.Glomerular diseasesReview
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Introduction: C3 glomerulopathy (C3G) is an ultrarare renal disease characterized by deposition of complement component C3 in the glomerular basement membrane (GBM). Rare and novel genetic variation in complement genes and autoantibodies to complement proteins are commonly identified in the C3G population and thought to drive the underlying complement dysregulation that results in renal damage. However, disease heterogeneity and rarity make accurately defining characteristics of the C3G population difficult. Methods: Here, we present a retrospective analysis of the Molecular Otolaryngology and Renal Research Laboratories C3G cohort. This study integrated complement biomarker testing and Results: The largest disease profiles of C3G included patients with autoantibodies to complement proteins (48%) and patients for whom no genetic and/or acquired drivers of disease could be identified (43%). The correlation between the stabilization of convertases by complement autoantibodies as measured by Conclusion: This study implicates complement autoantibodies as robust drivers of systemic complement dysregulation in approximately 50% of C3G but also highlights the need for continued discovery-based research to identify novel drivers of disease.
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Registered trials
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.