ABSTRACT
Renal impairment is a common complication in patients hospitalized in intensive care unit for acute respiratory distress syndrome (ARDS) due to COVID-19 infection. However, the prevalence of SARS-CoV-2 kidney injury is difficult to estimate worldwide. Several pathophysiological mechanisms are involved, including decreased renal perfusion related to mechanical ventilation, sepsis and cytokines release, as well as direct virus toxicity on proximal tubular cells and podocytes, mediated by angiotensin 2 conversion receptors (ACE 2) and TMPRSS proteases. More than 20 % of ICU COVID-19 patients require extra renal replacement therapy (ERT) for acute renal failure that is made difficult by the hypercoagulable state of these patients, responsible for filter thrombosis.