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The samples were then centrifuged at 21,000 g for 20 min at 4 C

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Deceased donors, particularly DCD and DBD donors, have higher level of complement activation as assessed by increased level of C3d, C4d, C5a, Bb or soluble C5b-9 ( Brain death exacerbates the detrimental effects of complement activation, and experimental complement inhibition by CR2-Crry in a mouse cardiac transplant model significantly reduced myocardial injury and prolonged graft survival ( Furthermore, as demonstrated by Burk et al., multiple trauma occurring in the donor results in a severe complementopathy, characterized by immediate activation, consumption, and dysfunction of the complement cascade, that may have consequences in transplantation perspective ( After organ procurement, the detrimental role of complement in renal IRI has been extensively investigated by experimental studies using C3, C5, and C6deficient murine model ( An emerging therapeutic strategy to arrest upstream complement activation is C1-esterase-inhibitor (C1- INH), an endogenous serine protease inhibitor of classical- and lectin pathway ( In a rat model of brain death, high-dose C1-INH treatment significantly improved renal function and reduced local and systemic inflammation, as assessed by lower serum creatinine level, decreased pro-inflammatory gene expression and serum IL-6 respectively ( To evaluate the effect of C1-INH (CINRYZE) as a donor pre-treatment strategy to decrease systemic inflammation and decrease the incidence of DGF in ECD, is currently the aim of phase I, randomized trial (NCT02435732) that is expected to be completed in May 2022

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The enzyme is a tetramer of identical subunits of 40 kDa