The exact pathogenesis is not fully elucidated. The hallmark feature is the formation of polyclonal IgG autoantibody against the P antigen, which is a polysaccharide surface antigen on red cells in most humans. As a weak, biphasic antibody, it absorbs to the P antigen in the<unk>  temperature as in the periphery in the primary phase, and fixes complement on recirculation to the core temperature in the secondary phase, resulting in intravascular hemolysis.
Paroxysmal cold hemoglobinuria
Paroxysmal nocturnal hemoglobinuria
Hereditary spherocytosis
Mixed autoimmune hemolytic anemia
Congenital hemolytic anemia
Trimethylaminuria
Hemoglobin Lepore syndrome
Hereditary persistence of fetal hemoglobin