ReviewPediatric nephrology (Berlin, Germany)2010
Genetics and complement in atypical HUS.
Review in Pediatric nephrology (Berlin, Germany), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 2 of them syntheses 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
76 citing papers in PubMed, 2 syntheses or guidelines pooled it, 152 citations in OpenAlex.
- Clinical Practice Guidelines for the Management of Atypical Hemolytic Uremic Syndrome in Korea.Journal of Korean medical science · 2016Guideline
- Diagnostic criteria for atypical hemolytic uremic syndrome proposed by the Joint Committee of the Japanese Society of Nephrology and the Japan Pediatric Society.Clinical and experimental nephrology · 2014Guideline
- Trial
- Navigating Pediatric Atypical Hemolytic Uremic Syndrome: A Two-Year Case Series From Eastern India.Cureus · 2025Article
- Plasminogen mutation-associated thrombotic microangiopathy and role of anticoagulation: a single institution case series.Research and practice in thrombosis and haemostasis · 2025Article
- Eculizumab is efficacious and safe in pediatric patients with various forms of hemolytic uremic syndrome: a retrospective clinical experience of a tertiary center.Frontiers in pharmacology · 2025Article
- The Inhibitory Effects of a Factor B-Binding DNA Aptamer Family Supersede the Gain of Function of Factor B Variants Associated with Atypical Hemolytic Uremic Syndrome.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Shiga toxin targets the podocyte causing hemolytic uremic syndrome through endothelial complement activation.Med (New York, N.Y.) · 2023Article
- Can eculizumab be an option in traditional treatment-resistant ulcerative colitis?Gastroenterology and hepatology from bed to bench · 2023Article
- Physiology and pathology of the C3 amplification cycle: A retrospective.Immunological reviews · 2023Review
- Subtypes and Mimics of Sepsis.Critical care clinics · 2022Review
- Atypical HUS and Crohn's disease-interference of intestinal disease activity with complement-blocking treatment.Pediatric nephrology (Berlin, Germany) · 2021Article
- Murine Factor H Co-Produced in Yeast With Protein Disulfide Isomerase Ameliorated C3 Dysregulation in Factor H-Deficient Mice.Frontiers in immunology · 2021Article
- Utilization Pattern for Eculizumab Among Children With Hemolytic Uremic Syndrome.Frontiers in pediatrics · 2021Article
- The interaction between the complement system and hemostatic factors.Current opinion in hematology · 2020Review
- Clinical and Pathogenic Correlations Between SARS-CoV-2 Infection and Hemolytic Uremic Syndrome in Children.Maedica · 2020Article
- COVID-19, microangiopathy, hemostatic activation, and complement.The Journal of clinical investigation · 2020Article
- Complement activity and complement regulatory gene mutations are associated with thrombosis in APS and CAPS.Blood · 2020Article
- Common Genetic Variants in the Complement System and their Potential Link with Disease Susceptibility and Outcome of Invasive Bacterial Infection.Journal of innate immunity · 2020Review
- Loss-of-Function Mutations in the CFH Gene Affecting Alternatively Encoded Factor H-like 1 Protein Cause Dominant Early-Onset Macular Drusen.Ophthalmology · 2019Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Central to the pathogenesis of atypical hemolytic uremic syndrome (aHUS) is over-activation of the alternative pathway of complement. Following the initial discovery of mutations in the complement regulatory protein, factor H, mutations have been described in factor I, membrane cofactor protein and thrombomodulin, which also result in decreased complement regulation. Autoantibodies to factor H have also been reported to impair complement regulation in aHUS. More recently, gain of function mutations in the complement components C3 and Factor B have been seen. This review focuses on the genetic causes of aHUS, their functional consequences, and clinical effect.
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.