Circulating level of Angiopoietin-2 is associated with acute kidney injury in coronavirus disease 2019 (COVID-19)

Excerpt

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 COVID-19 by a secondary thrombotic microangiopathy (TMA) phenomenon, as evidenced by low ADAMTS13 activity to von Willebrand factor (VWF:Ag) ratio [7]. However, the mechanism by which AKI occurs in COVID-19 has yet to be fully elucidated. …