Mechanisms of Kidney Damage Development in Patients with New Coronavirus Infection: Literature Review

Abstract

Every fourth person in the world currently has kidney problems to one or another degree. It is known that the novel coronavirus infection (COVID-19) is primarily a respiratory disease, but the kidney is a target organ. The coronavirus is tropic to kidney tissue due to the presence in the organ of RNA of angiotensin-converting enzyme type 2 and transmembrane serine protease 2, which is considered to be a target of this virus. The presence of renal failure in any stage is an independent unfavorable risk factor for contracting coronavirus and leads to a high frequency of hospitalization and mortality rate. Kidney failure is caused by various pathogenetic mechanisms: the direct cytopathic effect of the virus on their structures (podocytes, mesangial cells in the renal corpuscle, capillary endothelium in the glomerulus, epithelial cells in the proximal tubules), cytokine storm, damage to the renin–angiotensin–aldosterone system, and immunothrombosis. In many patients with confirmed coronavirus infection, from the first days of the disease, laboratory tests show significant changes in urine analysis (hematuria, proteinuria) and increased level of creatinine in the blood serum. The development of acute kidney injury is a main mortality risk factor. More research is needed into the exact effects of SARS-CoV-2 on the kidneys. Understanding the main pathogenetic pathways of their damage in COVID-19 is necessary to develop strategies and effective treatments.