[Atypical hemolytic uremic syndrome].
By Y. Fujimura. [Rinsho ketsueki] The Japanese journal of clinical hematology, 2013
968 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/93f945532a1c6f81f2603db6043bf8027f22c507
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Citations in the corpus
- Genetics and outcome of atypical hemolytic uremic syndrome: a nationwide French series comparing children and adults. (2013, background): “In the last decade, aHUS has been linked to dysregulation of the alternative C3 convertase leading to complement-induced endothelial damage and ultimately thrombotic microangiopathy (1).”
- Three-dimensional reconstruction of protein networks provides insight into human genetic disease (2012, background): “An interesting example is the hemolytic uremic syndrome, which is associated with mutations on the corresponding interaction interfaces of both CFH and C3 that mediate the interaction between the two proteins 40 ( Supplementary Note 11 and Supplementary Fig.”
- Complement System Part II: Role in Immunity (2015, background): “Atypical hemolytic uremic syndrome is a renal thrombotic microangiopathy disease, characterized by glomerular microvascular endothelial cells activation and damage, leading to microthrombi formation andmechanical hemolysis (206).”
- Guidelines on the diagnosis and management of thrombotic thrombocytopenic purpura and other thrombotic microangiopathies (2012, background): “Increasingly, the role of complement defects in D , atypical HUS is being defined (Kavanagh & Goodship, 2010) and use of the complement inhibitor, eculizumab, appears successful in these cases (AlAkash et al, 2011; Riedl et al, 2011), but may also have a role in severe D+HUS (Lapeyraque et al,…”
- Complement System Part I – Molecular Mechanisms of Activation and Regulation (2015, background): “Without appropriate treatment, it leads to end stage renal disease in approximately 60% of patients (313, 314).”
- ADAMTS13 and von Willebrand Factor in Thrombotic Thrombocytopenic Purpura (2015, background): “Approximately 60% of patients with aHUS have been shown to have mutations in complement regulatory proteins (65), including complement factor H (CFH, ~25%), factor I (CFI, 5–10%), and membrane cofactor protein (MCP, ~10%), or in complement proteins C3 and factor B (2– 10%).”