Covid-19急性肾损伤机制审查

L. Maltseva, I. Vasalatii, Y. Isaakyan, O. Morozova
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引用次数: 1

摘要

COVID-19急性肾损伤(AKI)最重要的特征是缺乏单一的主要发病环节。深入了解疾病发病机制和主要环节,有助于发现AKI的早期标志物,有助于COVID-19患者的早期诊断、预后、个性化治疗和预防肾损害。目的:总结COVID- 19中AKI已知机制的临床和科学研究数据。目的:确定COVID-19患者早期肾损伤标志物。材料和方法。在Web of Science、Scopus和RSCI数据库中,我们选择了81个来源,这些来源包含了与本综述主题相关的临床和科学研究的相关数据。结果:报道的COVID-19患者肾损害的主要机制为:细胞内病毒活性导致细胞死亡、促炎细胞因子和细胞因子风暴过度释放、肾素-血管紧张素-醛固酮系统(RAAS)病理、超能性炎症和免疫血栓形成。在RAAS失调的情况下,血管紧张素II的主要作用,以及促炎症细胞因子的谱和它们在细胞因子风暴发展中的功能被确定。考虑到SARS-CoV-2对肾上皮的直接细胞病变作用可能是COVID-19患者AKI的独立原因。超能炎症反应与免疫血栓形成过程之间的关系,这是由许多防御系统介导的,包括中性粒细胞、血小板和补体系统的蛋白质。分析COVID-19患者肾血管血栓性并发症的风险。我们还分析了COVID-19肾脏损伤的潜在早期生物标志物,并与AKI的临床生物标志物进行了比较。结论:AKI是COVID-19危重症患者最常见的并发症之一,明显恶化疾病预后。对肾损伤机制的研究有助于发现早期诊断、病程预后和进一步确定最佳个性化治疗所需的新标志物。©2021 JSC Vidal Rus。版权所有。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.
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来源期刊
Nephrology and Dialysis
Nephrology and Dialysis Medicine-Nephrology
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