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Glomerulonephritis characterized by C3 accumulation with little or absent deposition of immunoglobulin, in the absence of ultrastructural electron-dense transformation seen in dense deposit disease.
Features include always present findings: Microscopic hematuria, Glomerular C3 deposition, and Glomerular subendothelial electron-dense deposits; and very common findings: Mesangial matrix expansion, Mesangial hypercellularity, and Thickening of glomerular capillary wall. 9 total HPO annotations.
Organ System | Phenotype Count | Example Features |
|---|---|---|
Kidneys and urinary system | 7 | Glomerulonephritis, Stage 5 chronic kidney disease, Thickening of glomerular capillary wall |
CFHR5 encodes complement factor H related 5 (569 aa). Involved in complement regulation. The dimerized forms have avidity for tissue-bound complement fragments and efficiently compete with the physiological complement inhibitor CFH Highest expression in Liver (39.2 TPM) and Testis (0.1 TPM).
C3 glomerulonephritis is associated with mutations in the CFHR5 gene on chromosome 1.
CFHR5 is classified as a druggable target (Druggable Genome category) with score 0.0.
Genetic testing for CFHR5 is available. Testing is considered confirmatory for diagnosis.
Biomarker and diagnostic research for C3 glomerulonephritis has been reported in the published literature.
Phenotype severity distribution: 3 always present features, 3 very common features, 1 common feature.
3 clinical trials registered, 1 recruiting. Interventions under study include drug therapy. Pipeline includes 1 PHASE3, 2 PHASE2. Research is sponsored by a mix of industry and academic institutions.
81 publications have been identified in PubMed for C3 glomerulonephritis. Research spans Case Report / Case Series (33%), Review / Meta-Analysis (21%), and Basic Science / Preclinical (15%).
Research Type | Count | % of Total |
|---|---|---|
Patient case studies | 27 |
Data assembled from 7 of 12 sources · Last updated Sep 19, 2026, 11:54 PM UTC
Online Mendelian Inheritance in Man
European rare disease database
Genetic and Rare Diseases Info Center
Common questions about C3 glomerulonephritis
Research summaries | 17 | 21% |
Laboratory research | 12 | 15% |
Disease patterns and progression | 10 | 12% |
Testing and diagnosis research | 7 | 9% |
Clinical study results | 4 | 5% |
New treatment approaches | 4 | 5% |
Ayehu G (2026). [PMID: 39536144](https://pubmed.ncbi.nlm.nih.gov/39536144/). *Unknown Journal*. [Review / Meta-Analysis]
Praga M (2026). [PMID: 41921739](https://pubmed.ncbi.nlm.nih.gov/41921739/). *Am J Kidney Dis*. [Review / Meta-Analysis]
Gödecke V (2026). [PMID: 42012503](https://pubmed.ncbi.nlm.nih.gov/42012503/). *Inn Med (Heidelb)*. [Review / Meta-Analysis]
Alrasheed R (2026). [PMID: 41884136](https://pubmed.ncbi.nlm.nih.gov/41884136/). *Front Med (Lausanne)*. [Case Report / Case Series]
Chati P (2026). [PMID: 40954329](https://pubmed.ncbi.nlm.nih.gov/40954329/). *Pediatric nephrology (Berlin, Germany)*. [Epidemiology / Natural History]
Stroppou P (2026). [PMID: 42004655](https://pubmed.ncbi.nlm.nih.gov/42004655/). *Kidney Med*. [Case Report / Case Series]
Cetin TE (2026). [PMID: 41654355](https://pubmed.ncbi.nlm.nih.gov/41654355/). *Nefrologia*. [Case Report / Case Series]
Dixon BP (2026). [PMID: 42138781](https://pubmed.ncbi.nlm.nih.gov/42138781/). *Adv Ther*. [Clinical Trial Publication]
Filippone EJ (2026). [PMID: 41767602](https://pubmed.ncbi.nlm.nih.gov/41767602/). *Frontiers in nephrology*. [Review / Meta-Analysis]
Khullar V (2026). [PMID: 41525388](https://pubmed.ncbi.nlm.nih.gov/41525388/). *Kidney & blood pressure research*. [Diagnostic / Biomarker]
AI-curated news mentioning C3 glomerulonephritis
Updated Jun 12, 2026
A recent case-based review highlights that glomerulonephritis in Takayasu arteritis is primarily characterized by mesangial and AA amyloid lesions, often occurring during remission. This insight could inform future research and treatment strategies for affected patients.
A case report highlights IgA-dominant infection-related glomerulonephritis linked to Mycobacterium avium. This discovery adds to the understanding of rare kidney diseases associated with specific infections.
New research highlights C3-dominant glomerulonephritis as a potential indicator of underlying autoinflammatory diseases. This discovery could lead to improved diagnostic strategies for patients presenting with nephritic symptoms.