In healthy individuals, complement is used to attack foreign substances, and the complement system is highly regulated to prevent it from damaging healthy tissues and organs. However, in most patients with<unk> , it has been demonstrated that chronic, uncontrolled, and excessive activation of complement can result from production of anti-factor H autoantibodies or from genetic mutations in any of several complement regulatory proteins (e.g., factor H, factor HR1 or HR3, membrane cofactor protein, factor I, factor B, complement C3, and thrombomodulin). This results in platelet activation, damage to endothelial cells (cells that line the blood vessels), and white blood cell activation, leading to systemic TMA, which manifests as decreased platelet count, hemolysis (breakdown of red blood cells), damage to multiple organs, and often, death.
Atypical hemolytic uremic syndrome
Thrombotic thrombocytopenic purpura
Hemolytic–uremic syndrome
Post-transfusion purpura
Severe fever with thrombocytopenia syndrome
Cold autoimmune hemolytic anemia
Transfusion-dependent anemia
Immune reconstitution inflammatory syndrome