COVID-19后肾脏的病理、结构和功能改变

L. Kamyshnikova, O. Efremova, D. S. Pisankina, K. S. Gorbachevskaya, Alexander N. Pishchanskiy, M. S. Sviridova
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摘要

现在有越来越多的证据表明COVID-19的长期影响,影响几乎所有人体系统和器官,包括肾脏。本文的目的是研究COVID-19感染患者肾脏的病理、结构和功能变化。材料和方法。文章在PubMed、Medline、谷歌学术、电子图书馆、临床试验数据库中检索,关键词为“后冠状病毒综合征”、“肾损害(肾脏疾病)”、“COVID-19”、“SARS-CoV-2”和“肾小球肾炎”,中文和英文。研究使用了截至2022年9月28日公布的报告先前冠状病毒感染后可检测到肾损害病例的数据库。本综述包括文献综述、临床病例和报告先前确诊的COVID-19后可检测到肾损害确诊病例的原始研究。排除了冠状病毒感染急性期仅关注肾脏损害的来源。结果。主要的病毒损伤是通过对血管紧张素转换酶-2 (ACE-2)受体的影响进行的。同样重要的病毒损伤机制是免疫和炎症反应,补体系统功能障碍,导致多器官功能衰竭。冠状病毒感染对肾脏的长期影响表现为肾小球滤过率(eGFR)降低、肌酐水平升高、蛋白尿和微量血尿。Dickkopf-3蛋白(uDKK-3)可能成为一种有希望的肾脏损伤标志物。COVID-19后肾脏疾病既可以从头发生,也可以与先前的COVID-19肾脏并发症一起发生。肾损害最常见的形态变异是肾小管病变和肾小球肾炎的各种形态变异。结论。COVID-19与COVID-19后肾损害的关联得到了常见发病机制的支持,包括病毒通过ACE-2的直接损害、机体的炎症和免疫反应。这些数据得到了COVID-19感染患者肾组织炎症和损伤的可检测标志物、肾实质坏死和纤维化的形态学图像的证实。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pathogenetic and structural and functional changes in the kidneys after COVID-19
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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