Abstract
There is now a growing evidence of the long-term effects of COVID-19, affecting almost all human systems and organs, including the kidneys. The objective of this paper was to study pathogenetic and structural and functional changes in the kidneys in patients with COVID-19 infection. Materials and methods. Articles were searched in PubMed, Medline, Google Scholar, E-library, Clinical Trial databases using the keywords "post-COVID syndrome," "renal damage (kidney disease)," "COVID-19," "SARS-CoV-2," and "glomerulonephritis" in Russian and English. Databases reporting cases of detectable renal damage following a prior coronavirus infection published by September 28, 2022 were used. This review includes literature reviews, clinical cases, and original studies reporting the confirmed cases of detectable renal damage after confirmed prior COVID-19. The sources that focus only on renal damage during the acute period of coronavirus infection have been excluded. Results. Primary viral damage is carried out through the effect on the receptors of angiotensin-converting enzyme-2 (ACE-2). No less important mechanisms of viral damage are immunological and inflammatory reactions, dysfunctions of the complement system, leading to multiple organ failure. The long-term consequences of coronavirus infection on the kidneys were manifested in a decrease in the estimated glomerular filtration rate (eGFR), an increase in creatinine levels, proteinuria, and microhematuria. Dickkopf-3 protein (uDKK-3) may become a promising marker of kidney damage. Post-COVID renal disease can occur both de novo and with a previous renal complication of COVID-19. The most common morphological variants of kidney damage were tubular lesions and various morphological variants of glomerulonephritis. Conclusion. The association of COVID-19 and kidney damage in the post-COVID period is supported by common mechanisms of pathogenesis, including direct viral damage through ACE-2, inflammatory and immune reactions of the body. These data are confirmed by detectable markers of inflammation and damage to the renal tissue, the morphological picture of necrosis, fibrosis of the renal parenchyma in patients with COVID-19 infection.
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