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Recent evidence suggests that signs and symptoms of severe COVID-19 infection resemble more the pathophysiology and phenotype of complement-mediated thrombotic micoangiopathies (TMA), rather than sepsis-induced coagulopathy or disseminated intravascular coagulation (DIC) (Campbell and Kahwash 2020, Zhang, et al 202. Since effective treatment is available for complement-mediated TMA (Gavriilaki 202, we aim to systematically describe relevant features (clinical phenotype, pathophysiology and management) in patients with severe COVID