ArticleAnnals of blood2023
Atypical hemolytic uremic syndrome: genetically-based insights into pathogenesis through an analysis of the complement regulator CD46.
Article in Annals of blood, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
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Who cites it
5 citing papers in PubMed.
- Influenza A(H1N1) triggered atypical hemolytic uremic syndrome in a child with homozygous CD46 variant successfully treated with ravulizumab: a case report.CEN case reports · 2026Article
- Renal-Limited Thrombotic Microangiopathy in Infants: A Case Series.Kidney medicine · 2026Article
- A review of genetic and epigenetic biomarkers involved in the occurrence of atypical hemolytic uremic syndrome and its therapeutic strategies.Molecular biology reports · 2026Review
- Introductory comments about the special series of thrombotic microangiopathy.Annals of blood · 2024Article
- The Rationale of Complement Blockade of the MCPInternational journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The complement system is a critical innate immune defense mechanism that also facilitates antigen recognition as well as antibody production through the adaptive immune response. Overall, complement activation contributes to the immune system's recognition and response to foreign pathogens and altered self. Regulating complement activation, particularly its powerful alternative pathway (AP) amplification loop, plays a key role in modulating tissue damage at sites of injury. Besides a predisposition to infections and autoimmunity (particularly systemic lupus erythematosus) in individuals deficient in activating components, variants in complement regulators are associated with multiple diseases including atypical hemolytic uremic syndrome (aHUS), paroxysmal nocturnal hemoglobinuria (PNH), and age-related macular degeneration (AMD). In particular, the pathogenesis of aHUS is commonly related to a rare heterozygous loss-of-function (LOF) mutation in the gene for complement factor H (
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Registered trials
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