Potential targets for preclinical diagnostics of acute kidney injury in covid-19 patients (review of literature).

An relevance of the topic was defined by the high occurrence, unfavorable prognosis, lack of diagnostic techniques for early stages of acute kidney injury (AKI) disclosed in patients with COVID-19 (Coronavirus Disease 2019). Screening of medical literature for selection of AKI preclinical biomarkers was considered as main aim of this review. More than 200 publications from Russian Science Citation Index (RSCI), Scopus, The Cochrane Library, and MEDLINE were reviewed. Such risk factors as hypoxemia, increased intrathoracic pressure associated with Acute Respiratory Distress Syndrome (ARDS), hypertension (HT) involving endothelial dysfunction, and Diabetes mellitus were considered to be associated with AKI. There were explicated cytopathic and immune-mediated (cytokine-induced) mechanisms of COVID-19 associated AKI pathogenesis. Multiple methodological approaches were defined for detection and identification of the biomarkers based on urine proteome and metabolome screening. Perspective ways in the preclinical diagnostics of AKI such as detection of the markers of injury of the hypoxia-sensitive proximal canaliculi and the ATP metabolites that reflect first stages of the energy metabolism disorder in the epithelium lining canaliculi were identified in this study. The instantaneous and non-invasive investigation of different markers was regarded as possible method of the prognostication. The accuracy of the diagnosis on the initial stages of AKI, substantiate for preventive start of therapy, and make projections on the disease`s outcome will be improved due to the identification of high-sensitive specific biomarkers.

Mechanisms of acute kidney injury in Covid-19 Review

The most important feature of acute kidney injury (AKI) in COVID-19 is the absence of a single main link of pathogenesis. A thorough understanding of the mechanisms and main links of the pathogenesis of the disease will allow the identifi cation of early markers of AKI, which will contribute to early diagnosis, prognosis, personalized therapy and prevention of kidney damage in patients with COVID-19. Aim: to summarize data from clinical and scientifi c studies on the known mechanisms of AKI in COVID- 19. To identify markers of early kidney injury in COVID-19. Materials and methods. In the Web of Science, Scopus and RSCI databases, 81 sources were selected that contained relevant data from clinical and scientifi c researches on the topic of this review. Results: the main reported mechanisms of kidney damage in COVID-19 patients are as follows: intracellular activity of the virus leading to cell death, excessive release of pro-infl ammatory cytokines and cytokine storm, pathology of the renin-angiotensin-aldosterone system (RAAS), hyperergic infl ammation and immunothrombosis. The main effects of angiotensin II in the case of dysregulation of the RAAS, as well as the spectrum of pro-infl ammatory cytokines and their functions in the development of the cytokine storm, were determined. The possibility of a direct cytopathic effect of SARS-CoV-2 on the renal epithelium as an independent cause of AKI in COVID-19 was considered. The association between the hyperergic infl ammatory response and the process of immunothrombosis, which is mediated by many defense systems, including neutrophils, platelets and proteins of the complement system was presented. The risk of thrombotic complications in the renal vessels in patients with COVID-19 was anaysed. An analysis of potential early biomarkers of kidney injury in COVID-19 were also presented and compared with clinical biomarkers of AKI. Conclusions: AKI is one of the most common complications in critically ill patients with COVID-19, which signifi cantly worsens the prognosis of the disease. The study of the mechanisms of kidney injury contributes to the discovery of new markers necessary for early diagnosis, prognosis of the course of the disease, and further determination of the optimal personalized therapy. © 2021 JSC Vidal Rus. All Rights Reserved.