The aim kf this study is to understand Coronavirus disease 2019 (COVID-19)–associated coagulopathy, responsible for high rates of pulmonary thrombosis, is poorly characterized. Clinical studies identified several biomarkers, such as D-dimer. Different mechanisms have been proposed, including neutrophil and complement activation, vascular damage, and tissue factor expression. The intrinsic pathway of coagulation, which not only amplifies fibrin generation but also links to inflammation, including plasma kallikrein and bradykinin, both proposed to contribute to COVID-19, has not been studied. We performed a comprehensive analysis on the intrinsic pathway to characterize its role in COVID-19. By simultaneously studying potential triggers of the intrinsic pathway, we were able to identify neutrophils, neutrophil extracellular traps (NETs), and complement activation as potential drivers of this complex immunothrombotic disease. We included 228 consecutive patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) confirmed by real-time polymerase chain reaction (Table 1). Disease severity was classified as mild in patients not admitted to the hospital, moderate in admitted patients requiring oxygen via nasal cannula, and progressive/severe in patients requiring oxygen via a face mask, or admitted to the intensive care unit for invasive ventilation or those who died ≤7 days.


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