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

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

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 …

Mutations in the complement regulators factor H, membrane cofactor protein (MCP), and
factor I are associated with atypical hemolytic uremic syndrome (aHUS, MIM 235400) …

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 efficiency of the complement system as an innate immune defense mechanism depends
on a fine control that restricts its action to pathogens and prevents non-specific damage to …

Atypical hemolytic uremic syndrome (aHUS) is a disorder characterized by hemolytic
anemia, thrombocytopenia, and acute renal failure. Mutations, polymorphisms, and copy …

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 …

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 …

Factor H (FH) is the key regulator of the alternative pathway of complement. The carboxyl‐
terminal domains 19–20 of FH interact with the major opsonin C3b, glycosaminoglycans …