ABSTRACT
COVID-19 is a severe acute respiratory disease caused by the SARS-CoV-2 virus. Although COVID-19 is characterized mainly by diffuse alveolar damage and acute respiratory failure, in some cases COVID-19 may acquire extra-respiratory features, including renal dysfunction that has existed earlier or developed de novo. The reasons for the extra-respiratory manifestations are biological properties of SARS-CoV-2 based on its multiple organ tropism. It has been shown that at least 50% of patients hospitalized for COVID-19 have proteinuria, hematuria, and signs of renal dysfunction, which in some cases reaches the degree of acute kidney injury (AKI). Here we present a review that discusses the clinical aspects and possible pathophysiological mechanisms of kidney damage in COVID-19. It is believed that renal damage observed in this disease is the result of a complex mechanism induced directly or indirectly by SARS-CoV-2 with the development of acute kidney injury. Two main pathophysiological mechanisms of kidney damage in COVID-19 are discussed. The first of them is the direct cytopathic effect of SARS-CoV-2 on the renal epithelium with the development of acute tubulonecrosis. The second mechanism is the cytokine storm syndrome that results from hyperactivation of the immune system with the development of acute renal and multiorgan infl ammatory damage accompanied by hypoxia, persistent hypotension, rhabdomyolysis, hyperactivation of the coagulation cascade, and microcirculation disorders. From a clinical point of view, it should be noted that signs of kidney damage are associated with an increase in the severity of COVID-19 and a poor outcome of the disease, and the prognosis becomes the worst with the development of AKI (the risk of death may increase by 5.3 times). The incidence of COVID-19 in patients with ESRD is higher than in the general population. The most typical for these patients is a severe course of the disease, which determines the increased mortality in comparison with the general population, caused by a respiratory failure with hyperactive infl ammation, cytokine storm, hemodynamic, and multiple organ failures. © 2021 JSC Vidal Rus. All rights reserved.