References

nid

Нефрология и диализ

Nephrology and Dialysis

1680-44222618-9801

Российское диализное общество

10.28996/2618-9801-2021-3-352-365

nid-37

Research Article

ОБЗОРЫ И ЛЕКЦИИ

REVIEWS AND LECTURES

Механизмы острого повреждения почек при Covid-19. Обзор

Mechanisms of acute kidney injury in Covid-19. Review

Мальцева

Л. Д.

Maltseva

L. D.

noemail@neicon.ru

Васалатий

И. М.

Vasalatii

I. M.

noemail@neicon.ru

Исаакян

Ю. А.

Isaakyan

Y. A.

noemail@neicon.ru

Морозова

О. Л.

Morozova

O. L.

morozova_ol@list.ru

ФГАОУ ВО «Первый МГМУ им. И.М. Сеченова» Минздрава РоссииРоссияI.M. Sechenov First Moscow State Medical UniversityRussian Federation

2021

21062024

233352365

2024

Мальцева Л.Д., Васалатий И.М., Исаакян Ю.А., Морозова О.Л.

Maltseva L.D., Vasalatii I.M., Isaakyan Y.A., Morozova O.L.

Данная работа распространяется под лицензией Creative Commons Attribution 4.0.

This work is licensed under a Creative Commons Attribution 4.0 License.

https://journal.nephro.ru/jour/article/view/37

Важнейшая особенность острого повреждения почек (ОПП) при новой коронавирусной инфекции (COVID-19) - отсутствие единого ведущего звена патогенеза. Глубокое понимание механизмов и основных звеньев патогенеза заболевания позволит определить ранние маркёры ОПП, что будет способствовать ранней диагностике, прогнозированию, персонифицированной терапии и профилактике повреждения почек у пациентов с COVID-19. Цель обзора: обобщить данные клинических и научных исследований по известным механизмам ОПП при COVID-19. Определить маркёры раннего повреждения почек при COVID-19. Материалы и методы: в базах данных Web of Science, Scopus и РИНЦ отобрали 81 релевантный источник, содержавший актуальные данные клинических и научных исследований по теме данного обзора. Результаты: отмечены основные механизмы повреждения почек при COVID-19: внутриклеточная активность вируса, приводящая к клеточной гибели, избыточное высвобождение провоспалительных цитокинов и цитокиновый шторм, патология ренин-ангиотензин-альдостероновой системы (РААС), гиперергическое воспаление и иммунотромбоз. Определены основные эффекты ангиотензина II при нарушении регуляции РААС, а также спектр провоспалительных цитокинов и их функций в развитии цитокинового шторма. Рассмотрена возможность прямого цитопатического действия SARS-CoV-2 на почечный эпителий как самостоятельной причины ОПП при COVID-19. Представлена взаимосвязь между гиперергической воспалительной реакцией и процессом иммунотромбоза, которая опосредована действием множества защитных систем организма, в том числе нейтрофилами, тромбоцитами и белками системы комплемента. Оценен риск тромботических осложнений в почечных сосудах у пациентов с COVID-19. Также представлен анализ потенциальных ранних биомаркёров повреждения почек при COVID-19 и сравнили их с клиническими биомаркёрами ОПП. Заключение: ОПП - одно из наиболее частых осложнений у тяжелобольных пациентов с COVID-19, которое значительно ухудшает прогноз течения болезни. Изучение механизмов повреждения почек способствует открытию новых маркёров, необходимых для ранней диагностики, прогнозирования течения болезни и дальнейшего выбора оптимальной персонифицированной терапии.

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 identification 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 scientific 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 scientific 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-inflammatory cytokines and cytokine storm, pathology of the renin-angiotensin-aldosterone system (RAAS), hyperergic inflammation and immunothrombosis. The main effects of angiotensin II in the case of dysregulation of the RAAS, as well as the spectrum of pro-inflammatory 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 inflammatory 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 significantly 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.

острое повреждение почекCOVID-19иммунотромбозбиомаркерыцитокиновый штормacute kidney injuryCOVID-19immunothrombosisbiomarkerscytokine storm

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The authors declare that there are no conflicts of interest present.