Emerging evidence suggests that endothelial dysfunction plays a central role in the pathophysiology of coronavirus disease 2019 (COVID-19). Recent post-mortem studies have documented extensive endothelial damage and inflammatory infiltrates in pulmonary and extra-pulmonary capillary beds of COVID-19 patients [1, 2]. This results in loss of endothelial integrity, activation of pro-coagulant pathways, disruption of the alveolar-capillary barrier, and vascular hyperpermeability [2]. Endothelial damage is a common denominator of thrombosis (micro-and macrovascular), acute respiratory distress syndrome (ARDS), acute kidney injury (AKI), and multiorgan failure (MOF), which are major drivers of morbidity and mortality in COVID-19 patients [3]. AKI is a common feature of COVID-19, impacting nearly half of all hospitalized patients, and is associated with high mortality, especially among those requiring renal replacement therapy [4–6]. We have recently shown that AKI may be driven in