ArticleFrontiers in immunology2022
Complement Factor I Variants in Complement-Mediated Renal Diseases.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Complete Complement Factor I (CFI) deficiency: a systematic review of forty-nine patients including three novel cases.BMC immunology · 2025Pooled it
- C3 Glomerulopathy Diagnosis, Current Treatments, and Emerging Therapies.Kidney medicine · 2026Review
- A young woman with membranoproliferative glomerulonephritis and persistent hypocomplementemia: a case report.BMC nephrology · 2026Article
- Actinomycotic Cholecystitis and Pancreatitis: Report of an Unusual Case.The American journal of case reports · 2026Article
- SARS-CoV-2 enhances complement-mediated endothelial injury via the suppression of membrane complement regulatory proteins.Emerging microbes & infections · 2025Article
- IgA Nephropathy With Membranoproliferative Pattern and Resistance to Immunosuppressive Therapy in Two Patients With Cofactor I Pathogenic Variant.Nephrology (Carlton, Vic.) · 2025Article
- Transcriptomics and proteomics reveal associations between myometrium and intrauterine adhesions.BMC women's health · 2025Article
- Targeted Complement Treatments in Glomerulopathies: A Comprehensive Review.Journal of clinical medicine · 2025Review
- CAMK2D and Complement Factor I-Involved Calcium/Calmodulin Signaling Modulates Sodium Iodate-Induced Mouse Retinal Degeneration.Investigative ophthalmology & visual science · 2025Article
- High prevalence of the hotspot complement factor I p.Ile357Met pathogenic variant in Tunisian atypical hemolytic uremic syndrome patients: report of three new cases and review of the literature.Frontiers in immunology · 2025Review
- Comprehensive functional characterization of complement factor I rare variant genotypes identified in the SCOPE geographic atrophy cohort.The Journal of biological chemistry · 2024Article
- A case-based narrative review of pregnancy-associated atypical hemolytic uremic syndrome/complement-mediated thrombotic microangiopathy.Kidney international · 2024Article
- Functional evaluation of rare variants in complement factor I using a minigene assay.Frontiers in immunology · 2024Article
- Urine Proteomics Link Complement Activation with Interstitial Fibrosis/Tubular Atrophy in Lupus Nephritis Patients.Seminars in arthritis and rheumatism · 2023Article
- Genetic variability shapes the alternative pathway complement activity and predisposition to complement-related diseases.Immunological reviews · 2023Review
- Article
- Immunological Characteristics of Chinese Adult Patients with Anti-Complement Factor H Autoantibodies-Associated Complement-Mediated Thrombotic Microangiopathy.Kidney diseases (Basel, Switzerland)Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
C3 glomerulopathy (C3G) and atypical hemolytic uremic syndrome (aHUS) are two rare diseases caused by dysregulated activity of the alternative pathway of complement secondary to the presence of genetic and/or acquired factors. Complement factor I (FI) is a serine protease that downregulates complement activity in the fluid phase and/or on cell surfaces in conjunction with one of its cofactors, factor H (FH), complement receptor 1 (CR1/CD35), C4 binding protein (C4BP) or membrane cofactor protein (MCP/CD46). Because altered FI activity is causally related to the pathogenesis of C3G and aHUS, we sought to test functional activity of select
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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.