Genetics of HUS: the impact of MCP, CFH, and IF mutations on clinical presentation, response to treatment, and outcome.

By J. Caprioli, M. Noris, S. Brioschi, G. Pianetti, F. Castelletti, P. Bettinaglio, C. Mele, E. Bresin, L. Cassis, S. Gamba and 8 more. Blood, 2006

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Atypical hemolytic uremic syndrome and C3 glomerulopathy: conclusions from a "Kidney Disease: Improving Global Outcomes" (KDIGO) Controversies Conference. (2017, background): “In many patients with an underlying complement risk factor, a trigger is required for aHUS to manifest.(12) Triggers include autoimmune conditions, transplants, pregnancy, infections, drugs, and metabolic conditions.”
Complement and coagulation: strangers or partners in crime? (2007, background): “Recently, it has been reported that symptoms of HUS are also present in patients carrying mutations in genes encoding other complement regulatory proteins, such as factor I and CD46 [ 62 ].”
Relative role of genetic complement abnormalities in sporadic and familial aHUS and their impact on clinical phenotype. (2010, methodology): “Moreover, we found unaffected carriers among relatives of both familial and sporadic cases, which confirms previous findings (5,15,27) that mutations in complement genes are predisposing rather than directly causal.”