Mechanisms of Kidney Damage Development in Patients with New Coronavirus Infection: Literature Review

Q4 Biochemistry, Genetics and Molecular Biology
E. V. Utkina, V. V. Novakovskaya, M. V. Egorova, N. V. Fomina, L. D. Chesnokova
{"title":"Mechanisms of Kidney Damage Development in Patients with New Coronavirus Infection: Literature Review","authors":"E. V. Utkina, V. V. Novakovskaya, M. V. Egorova, N. V. Fomina, L. D. Chesnokova","doi":"10.1134/s1990519x24700196","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Every fourth person in the world currently has kidney problems to one or another degree. It is known that the novel coronavirus infection (COVID-19) is primarily a respiratory disease, but the kidney is a target organ. The coronavirus is tropic to kidney tissue due to the presence in the organ of RNA of angiotensin-converting enzyme type 2 and transmembrane serine protease 2, which is considered to be a target of this virus. The presence of renal failure in any stage is an independent unfavorable risk factor for contracting coronavirus and leads to a high frequency of hospitalization and mortality rate. Kidney failure is caused by various pathogenetic mechanisms: the direct cytopathic effect of the virus on their structures (podocytes, mesangial cells in the renal corpuscle, capillary endothelium in the glomerulus, epithelial cells in the proximal tubules), cytokine storm, damage to the renin–angiotensin–aldosterone system, and immunothrombosis. In many patients with confirmed coronavirus infection, from the first days of the disease, laboratory tests show significant changes in urine analysis (hematuria, proteinuria) and increased level of creatinine in the blood serum. The development of acute kidney injury is a main mortality risk factor. More research is needed into the exact effects of SARS-CoV-2 on the kidneys. Understanding the main pathogenetic pathways of their damage in COVID-19 is necessary to develop strategies and effective treatments.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"37 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell and Tissue Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1134/s1990519x24700196","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 0

Abstract

Every fourth person in the world currently has kidney problems to one or another degree. It is known that the novel coronavirus infection (COVID-19) is primarily a respiratory disease, but the kidney is a target organ. The coronavirus is tropic to kidney tissue due to the presence in the organ of RNA of angiotensin-converting enzyme type 2 and transmembrane serine protease 2, which is considered to be a target of this virus. The presence of renal failure in any stage is an independent unfavorable risk factor for contracting coronavirus and leads to a high frequency of hospitalization and mortality rate. Kidney failure is caused by various pathogenetic mechanisms: the direct cytopathic effect of the virus on their structures (podocytes, mesangial cells in the renal corpuscle, capillary endothelium in the glomerulus, epithelial cells in the proximal tubules), cytokine storm, damage to the renin–angiotensin–aldosterone system, and immunothrombosis. In many patients with confirmed coronavirus infection, from the first days of the disease, laboratory tests show significant changes in urine analysis (hematuria, proteinuria) and increased level of creatinine in the blood serum. The development of acute kidney injury is a main mortality risk factor. More research is needed into the exact effects of SARS-CoV-2 on the kidneys. Understanding the main pathogenetic pathways of their damage in COVID-19 is necessary to develop strategies and effective treatments.

Abstract Image

新型冠状病毒感染患者肾损伤的发生机制:文献综述
摘要 目前世界上每四个人中就有一个人或多或少存在肾脏问题。众所周知,新型冠状病毒感染(COVID-19)主要是一种呼吸道疾病,但肾脏也是一个靶器官。由于肾脏组织中存在血管紧张素转换酶 2 型和跨膜丝氨酸蛋白酶 2 的 RNA,冠状病毒对肾脏组织具有趋性,而肾脏组织被认为是该病毒的靶器官。任何阶段的肾功能衰竭都是感染冠状病毒的一个独立的不利风险因素,并导致高住院率和高死亡率。肾衰竭由多种致病机制引起:病毒对肾脏结构(荚膜细胞、肾小球系膜细胞、肾小球毛细血管内皮细胞、近端肾小管上皮细胞)的直接细胞病理效应、细胞因子风暴、肾素-血管紧张素-醛固酮系统损伤和免疫血栓形成。在许多确诊感染冠状病毒的患者中,从发病的最初几天起,实验室检查就会显示尿液分析的显著变化(血尿、蛋白尿)和血清中肌酐水平的升高。急性肾损伤是主要的死亡风险因素。需要对 SARS-CoV-2 对肾脏的确切影响进行更多的研究。有必要了解 COVID-19 对肾脏造成损害的主要致病途径,以便制定策略和有效的治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Cell and Tissue Biology
Cell and Tissue Biology Biochemistry, Genetics and Molecular Biology-Cell Biology
CiteScore
0.80
自引率
0.00%
发文量
51
期刊介绍: The journal publishes papers on vast aspects of cell research, including morphology, biochemistry, biophysics, genetics, molecular biology, immunology. The journal accepts original experimental studies, theoretical articles suggesting novel principles and approaches, presentations of new hypotheses, reviews highlighting major developments in cell biology, discussions. The main objective of the journal is to provide a competent representation and integration of research made on cells (animal and plant cells, both in vivo and in cell culture) offering insight into the structure and functions of live cells as a whole. Characteristically, the journal publishes articles on biology of free-living and parasitic protists, which, unlike Metazoa, are eukaryotic organisms at the cellular level of organization.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信