Mechanisms of renal damage in patients with new coronavirus infection (literature review)

Abstract

One in four people in the world currently has kidney problems to varying degrees. It is known that the new coronavirus infection (COVID-19) is primarily a respiratory disease, but the kidneys are the target organ. Coronavirus is tropic to renal tissue due to the presence in the organ of the angiotensin converting enzyme type 2 and transmembrane serine protease 2, which are considered the target of this virus. The presence of any stage of renal insufficiency is an independent adverse risk factor for coronavirus infection and results in high hospitalization rates in hospitals and a mortality rate. Kidney damage is caused by a variety of pathogenetic mechanisms: direct cytopathic effect of the virus on their structure (in the kidney body - podocytes, mesangial cells, in the vascular glomerulus - endothelium of capillaries, in the proximal tubules - epithelial cells); cytokine storm; damage to the renin-angiotensin-aldosterone system; immunothrombosis. In many patients with confirmed coronavirus infection, significant changes in urine analysis (hematuria, proteinuria) and an increase in serum creatinine levels have been observed in the laboratory since the first days of the disease. One of the main risk factors for mortality is the development of acute renal injury. More research is needed on the exact effects of SARS-CoV-2 on the kidneys. Understanding the main pathogenetic pathways of kidney damage in COVID-19 is necessary for the development of strategies and the development of effective treatment methods.

Keywords

• coronavirus
• renal injury
• cytokine storm
• cytopathic effect
• renin-angiotensin-aldosterone system