Recent studies have identified mutations in the complement regulatory gene factor I (CFI)
that predispose to atypical hemolytic uremic syndrome (aHUS). CFI is a two-chain serine …

The complement system is regulated by inhibitors such as factor I (FI), a serine protease that
degrades activated complement factors C4b and C3b in the presence of specific cofactors …

Factor I (FI) is the major complement inhibitor that degrades C3b and C4b in the presence of
cofactors such as factor H (FH) and membrane cofactor protein (MCP). Recently, mutations …

Mutations in the plasma complement regulator factor H (CFH) and the transmembrane
complement regulator membrane co-factor protein (MCP) have been shown to predispose to …

Atypical hemolytic uremic syndrome (aHUS) associates with complement dysregulation
caused by mutations and polymorphisms in complement activators and regulators. However …

Genetic studies have shown that mutations of complement inhibitors such as membrane
cofactor protein, Factors H, I, or B and C3 predispose patients to atypical hemolytic uremic …

The pathogenesis of atypical hemolytic uremic syndrome (aHUS) is strongly linked to
dysregulation of the alternative pathway of the complement system. Mutations in …

Atypical hemolytic uremic syndrome (aHUS) is a rare disorder caused by dysregulation of
the complement alternative pathway, and associated with mutations in genes of complement …

Atypical hemolytic uremic syndrome (aHUS) is a disease of complement dysregulation. In
approximately 50% of patients, mutations have been described in the genes encoding the …

The hemolytic uremic syndrome is characterized by the triad of microangiopathic hemolytic
anemia, thrombocytopenia and acute renal failure. There are two general types. One occurs …