ArticleFrontiers in immunology2020
Factor H Autoantibodies and Complement-Mediated Diseases.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Variants in complement genes are uncommon in patients with anti-factor H autoantibody-associated atypical hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2023Pooled it
- Immunoglobulin Isotype Profiling of Anti-Factor H Autoantibodies in Complement-Mediated Diseases.International journal of laboratory hematology · 2026Article
- Complement Factor H as a Novel Predictive Biomarker for Deep Vein Thrombosis Recurrence: A Prospective Cohort Study.Journal of thrombosis and thrombolysis · 2026Article
- Updates in atypical hemolytic syndrome.Current opinion in pediatrics · 2026Review
- Actinomycotic Cholecystitis and Pancreatitis: Report of an Unusual Case.The American journal of case reports · 2026Article
- Article
- Primary membranoproliferative glomerulonephritis: natural history, pathogenesis, and treatment.Frontiers in nephrology · 2026Review
- Complement diagnostics and therapeutics for the pediatric population: early successes and opportunities for further advancement.Frontiers in pharmacology · 2026Review
- Update in the diagnosis of complement-mediated thrombotic microangiopathy/atypical hemolytic uremic syndrome.Hematology. American Society of Hematology. Education Program · 2025Review
- Article
- Acquired drivers of C3 glomerulopathy.Clinical kidney journal · 2025Review
- Effective long-term treatment with moss-produced factor H by overcoming the antibody response in a mouse model of C3G.Frontiers in immunology · 2025Article
- Complement-mediated HUS revisited: evolving insights into pathophysiology, diagnosis, and treatment.Frontiers in immunology · 2025Review
- Atypical hemolytic uremic syndrome: diagnosis, management, and discontinuation of therapy.Hematology. American Society of Hematology. Education Program · 2024Review
- Complement factor H in molecular regulation of angiogenesis.Medical review (2021) · 2024Review
- Global aHUS Registry Analysis of Patients Switching to Ravulizumab From Eculizumab.Kidney international reports · 2024Article
- Defining Nephritic Factors as Diverse Drivers of Systemic Complement Dysregulation in C3 Glomerulopathy.Kidney international reports · 2024Article
- Comprehensive Analysis of Thrombotic Microangiopathy Following Renal Transplantation.International journal of nephrology · 2024Article
- Atypical Hemolytic Uremic Syndrome: A Nationwide Colombian Pediatric Series.Global pediatric health · 2024Article
- Novel immunochromatographic test for rapid detection of anti-factor H autoantibodies with an assessment of its clinical relevance.Frontiers in immunology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Factor H (FH), a member of the regulators-of-complement-activation (RCA) family of proteins, circulates in human plasma at concentrations of 180-420 mg/L where it controls the alternative pathway (AP) of complement in the fluid phase and on cell surfaces. When the regulatory function of FH is impaired, complement-mediated tissue injury and inflammation occur, leading to diseases such as atypical hemolytic uremic syndrome (a thrombotic microangiopathy or TMA), C3 glomerulopathy (C3G) and monoclonal gammopathy of renal significance (MGRS). A pathophysiological cause of compromised FH function is the development of autoantibodies to various domains of the FH protein. FH autoantibodies (FHAAs) are identified in 10.9% of patients with aHUS, 3.2% of patients with C3G, and rarely in patients with MGRS. The phenotypic variability of FHAA-mediated disease reflects both the complexity of FH and the epitope specificity of FHAA for select regions of the native protein. In this paper, we have characterized FHAA epitopes in a large cohort of patients diagnosed with TMA, C3G or MGRS. We explore the epitopes recognized by FHAAs in these diseases and the association of FHAAs with the genetic deletion of both copies of the
Indexed as
Identifiers
What OpenQuestion holds
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.