Thrombotic microangiopathy after kidney transplantation: Expanding etiologic and pathogenetic spectra

Table 2 Etiology of post-transplant thrombotic microangiopathies

Recurrent TMA, rare (5%-10% of cases)

Mutations in complement regulatory factor genes [e.g., factor H, factor I, membrane cofactor protein, etc.]

Mutations in complement genes (e.g., C3)

TMA associated with autoantibodies (anti-factor H antibodies, anti-ADAMTS13 antibodies, antiphospholipid antibodies)

TMA associated with autoimmune diseases (scleroderma and systemic lupus erythematosus)

De-novo TMA, common (90%-95% of cases)

Associated with the type of donor and organ procurement procedure, e.g. Ischemia reperfusion injury

Drugs

I: Calcineurin inhibitors-associated TMA

II: Mammalian target of rapamycin inhibitors-associated TMA

Antibody-mediated rejection associated TMA

Infection-associated TMA

I: Viral, e.g. hepatitis C virus, parvovirus B19, and cytomegalovirus)

II: Fungal

III: Bacterial

Other rare causes, such as malignancy, other drugs, and pregnancy

ADAMTS13: A disintegrin-like and metalloprotease with thrombospondin type 1 motif, 13; TMA: Thrombotic microangiopathy.