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Table 2 Classification of TMA

From: Plasma exchange for thrombotic microangiopathy secondary to dermatomyositis associated with acute kidney injury and complement activation: a case report with literature review

 Infection with Shiga toxin–producing Escherichia coli or less frequently with Shigella dysenteriae. The most common cause of HUS in children.
 Deficiency of ADAMTS13 hereditary (Upshaw-Shulman syndrome) or acquired that causes by ADAMTS13 inhibitor.
aHUS, complement regulation abnormality
  Genetic mutations of complement proteins
  Autoantibodies against complement proteins, such as anti-factor H antibody
Secondary TMA
 Cobalamin metabolism disorder
  Chemotherapeutic agents (e.g., gemcitabine, mitomycin)
  Immunosuppressive agents (e.g., cyclosporine, tacrolimus)
  Antiplatelet agents (e.g., ticlopidine)
  Pneumococcus, human immunodeficiency virus, pertussis, influenza, varicella
 Preeclampsia/eclampsia, hemolysis, elevated liver HELLP
 Auto-immune disease, collagen disease
 Systemic lupus erythematosus, systemic sclerosis, polymyositis/dermatomyositis
 Bone marrow transplant, organ transplant-related