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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

STEC-HUS

 Infection with Shiga toxin–producing Escherichia coli or less frequently with Shigella dysenteriae. The most common cause of HUS in children.

TTP

 Deficiency of ADAMTS13 hereditary (Upshaw-Shulman syndrome) or acquired that causes by ADAMTS13 inhibitor.

aHUS, complement regulation abnormality

 Congenital

  Genetic mutations of complement proteins

 Acquired

  Autoantibodies against complement proteins, such as anti-factor H antibody

Secondary TMA

 Cobalamin metabolism disorder

 Drug-induced

  Chemotherapeutic agents (e.g., gemcitabine, mitomycin)

  Immunosuppressive agents (e.g., cyclosporine, tacrolimus)

  Antiplatelet agents (e.g., ticlopidine)

 Infection

  Pneumococcus, human immunodeficiency virus, pertussis, influenza, varicella

 Pregnancy-related

 Preeclampsia/eclampsia, hemolysis, elevated liver HELLP

 Auto-immune disease, collagen disease

 Systemic lupus erythematosus, systemic sclerosis, polymyositis/dermatomyositis

 Bone marrow transplant, organ transplant-related