Effects of coronavirus infection on markers of endothelial dysfunction in children with renal pathology

Abstract

Coronavirus infection (COVID-19), caused by severe acute respiratory syndrome 2 (SARS-CoV-2) RNA virus, has become a global problem in the world. Its consequences are of great importance for the health status of both adults and children, since the number of lethal outcomes and life-threatening complications has reached high rates. Of particular importance is coronavirus damage of important organs in childhood, due to the possible impairment of their functions and the development of later distant complications. Thus, the formation of acute kidney injury (AKI) in children is an independent risk factor for hospital mortality and disability. An important role in the development of this pathological condition is given to the development of endothelial dysfunction due to the activation of a number of pro-inflammatory cytokines and other biomarkers of endothelial disorders. Endothelitis, endothelial injury, endothelial cell dysfunction, and impaired microcirculatory function in various vascular beds all contribute markedly to life-threatening complications of COVID-19 such as venous thromboembolism and multiple organ failure. Endothelial dysfunction is the main determinant of microvascular disorders due to a shift in vascular balance towards greater vasoconstriction and subsequent organ ischemia, inflammation with concomitant tissue edema and procoagulant condition. In general, understanding the mechanisms of endothelial activation and dysfunction during COVID-19 infection can contribute to early detection of individuals, especially children, at risk of severe complications. Further study of endothelial dysfunction in the pathogenesis of AKI in children with COVID-19 is promising to determine a personalized approach to the management of pediatric patients with COVID-19.