ArticleJournal of the American Society of Nephrology : JASN2015
Variants in Complement Factor H and Complement Factor H-Related Protein Genes, CFHR3 and CFHR1, Affect Complement Activation in IgA Nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.
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Who cites it
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 153 citations in OpenAlex.
- Risk factors for recurrent IgA nephropathy after renal transplantation: A meta-analysis.Biomolecules & biomedicine · 2023Pooled it
- Complement-Regulatory Proteins CFHR1 and CFHR3 and Patient Response to Anti-CD20 Monoclonal Antibody Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Trial
- Serum complement C3 as a candidate biomarker for monitoring progression from chronic kidney disease to kidney failure.International urology and nephrology · 2026Article
- From Susceptibility Loci to Therapeutic Targets: The Genetic Architecture of IgA Nephropathy.International journal of molecular sciences · 2026Review
- Complement and kidney diseases: unlocking the opportunity of targeted treatments for glomerular diseases, including IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2026Review
- Extended haplotypes at the complement factor H gene locus are associated with liver transplant rejection.Hepatology communications · 2026Article
- Plasma Proteomics in IgA Nephropathy: From Circulating Biomarkers to Molecular Endotypes.Cells · 2026Review
- Association of Complement Genetics with Outcomes in IgA Nephropathy.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- IgA nephropathy new therapies: from data in adults to application in children.Pediatric nephrology (Berlin, Germany) · 2026Review
- Comprehensive Analysis of IgA Nephropathy Causal Factors in Plasma Proteins, Immune Cell Types, and Immune Cell Traits.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- Complement factor H supplementation rather than complete C3 knockout provides therapeutic benefits in IgA nephropathy.Molecular biomedicine · 2026Article
- TheOphthalmology science · 2026Article
- Breaking tolerance in the glomerulus: complement as a driver and therapeutic target in IgA nephropathy.Frontiers in medicine · 2026Review
- Gut microbiota dysbiosis and immune responses: insights from IgA nephropathy and inflammatory bowel disease.Frontiers in immunology · 2026Review
- Complement proteins associated with circulatory and glomerular IgA-containing immune complexes in patients with IgA nephropathy.Scientific reports · 2025Article
- Comprehensive genetic analysis and genotype-phenotype correlations in pediatric patients with atypical hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2025Article
- Review
- Evaluation of Serum Complement Components in Pediatric IgA Vasculitis: A Case-Control Study.Children (Basel, Switzerland) · 2025Article
- Exploring the mediating role of immune cells in the pathogenesis of IgA nephropathy through the inflammatory axis of gut microbiota from a genomic perspective.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- The pathogenesis of IgA nephropathy and implications for treatment.Nature reviews. Nephrology · 2025Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Complement activation is common in patients with IgA nephropathy (IgAN) and associated with disease severity. Our recent genome-wide association study of IgAN identified susceptibility loci on 1q32 containing the complement regulatory protein-encoding genes CFH and CFHR1-5, with rs6677604 in CFH as the top single-nucleotide polymorphism and CFHR3-1 deletion (CFHR3-1∆) as the top signal for copy number variation. In this study, to explore the clinical effects of variation in CFH, CFHR3, and CFHR1 on IgAN susceptibility and progression, we enrolled two populations. Group 1 included 1178 subjects with IgAN and available genome-wide association study data. Group 2 included 365 subjects with IgAN and available clinical follow-up data. In group 1, rs6677604 was associated with mesangial C3 deposition by genotype-phenotype correlation analysis. In group 2, we detected a linkage between the rs6677604-A allele and CFHR3-1∆ and found that the rs6677604-A allele was associated with higher serum levels of CFH and lower levels of the complement activation split product C3a. Furthermore, CFH levels were positively associated with circulating C3 levels and negatively associated with mesangial C3 deposition. Moreover, serum levels of the pathogenic galactose-deficient glycoform of IgA1 were also associated with the degree of mesangial C3 deposition in patients with IgAN. Our findings suggest that genetic variants in CFH, CFHR3, and CFHR1 affect complement activation and thereby, predispose patients to develop IgAN.
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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.