COVID-19-associated glomerulopathy and high-risk APOL1 genotype; Basis for a two-hit mechanism of injury? A narrative review on recent findings

Q4 Medicine
A. Pezeshgi, M. Mubarak, A. Djamali, Leila Mostafavi, S. Moghadam-Kia, Niloufar Alimohammadi, P. Peymani, Saharnaz Pezeshgi
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引用次数: 0

Abstract

Kidney is one of the most common organs affected by coronavirus disease 2019 (COVID-19) after the respiratory and immune systems Among the renal parenchymal components, the tubulointerstitial compartment is presumed to be the prime target of injury in COVID-19 The main mechanism of renal tubular damage by COVID-19 is considered to be indirect, i e , cytokine-mediated injury A proportion of infected individuals mount a strong inflammatory response to the virus by an exaggerated immune response of the body, namely cytokine storm Sudden and massive release of cytokines may lead to serious systemic hyper-inflammation and renal tubular injury and inflammation resulting in acute renal failure In addition, a number of cases of glomerulopathies, particularly collapsing glomerulopathy (CG) have been reported, predominantly in people of African ancestry, as a rare form of kidney involvement by SARS-CoV-2 that may originate from the background genetic susceptibility in this population complicated by the second hit of SARS-CoV-2 infection, either directly or indirectly It is noteworthy that renal injury in COVID-19 could be severe in individuals of African origin due to the aforementioned genetic susceptibility, especially the presence of high-risk apolipoprotein L1 (APOL1) genotypes Although the exact mechanism of kidney injury by SARS-CoV-2 is as yet unknown, multiple mechanisms are likely involved in renal damage caused by this virus This review was aimed to summarize the salient points of pathogenesis of kidney injury, particularly glomerular injury in COVID-19 disease in the light of published data A clear understanding of these is imperative for the proper management of these cases For this review, a search was made of Google Scholar, Web of Science, Scopus, EBSCO and PubMed for finding English language articles related to COVID-19, kidney injury and glomerulopathy From the information given in finally selected papers, the key aspects regarding glomerular involvement in COVID-19 were drawn out and are presented in this descriptive review [ABSTRACT FROM AUTHOR] Copyright of Journal of Nephropathology is the property of Isfahan University of Medical Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission However, users may print, download, or email articles for individual use This abstract may be abridged No warranty is given about the accuracy of the copy Users should refer to the original published version of the material for the full abstract (Copyright applies to all Abstracts )
COVID-19相关肾小球疾病和高危APOL1基因型;两次撞击伤害机制的依据是什么?对最近发现的叙述性综述
肾脏是继呼吸系统和免疫系统之后受2019冠状病毒病(新冠肺炎)影响最常见的器官之一。在肾实质成分中,肾小管间质室被认为是新冠肺炎损伤的主要靶点。新冠肺炎对肾小管损伤的主要机制被认为是间接的,细胞因子介导的损伤一定比例的感染者通过身体的过度免疫反应对病毒产生强烈的炎症反应,即细胞因子风暴细胞因子的突然大量释放可能导致严重的全身性炎症和肾小管损伤,并导致急性肾衰竭,特别是塌陷性肾小球病(CG)已被报道,主要发生在非洲血统的人身上,是严重急性呼吸系统综合征冠状病毒2型罕见的肾脏受累形式,可能源于该人群的背景遗传易感性,并因严重急性呼吸系统冠状病毒2型感染的第二次发作而复杂化,直接或间接值得注意的是,由于上述遗传易感性,尤其是高风险载脂蛋白L1(APOL1)基因型的存在,新冠肺炎患者的肾损伤在非洲血统的个体中可能严重。尽管SARS-CoV-2肾损伤的确切机制尚不清楚,多种机制可能与该病毒引起的肾损伤有关这篇综述旨在根据已发表的数据总结肾损伤,特别是新冠肺炎疾病肾小球损伤的发病机制要点。对这些机制的清楚理解对于这些病例的正确管理至关重要,科学网、Scopus、EBSCO和PubMed,用于查找与新冠肺炎、肾损伤和肾小球疾病相关的英文文章。从最终选择的论文中提供的信息,新冠肺炎肾小球受累的关键方面已被提取出来,并在本描述性评论中介绍[作者摘要]《肾脏病理学杂志》版权归伊斯法罕医学科学大学所有,未经版权持有人明确书面许可,其内容不得复制或通过电子邮件发送到多个网站或发布到listserv。然而,用户可以打印、下载或通过电子邮件发送文章供个人使用。本摘要可能会被删节。对副本的准确性不作任何保证。完整摘要用户应参考材料的原始出版版本(版权适用于所有摘要)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Nephropathology
Journal of Nephropathology Medicine-Nephrology
CiteScore
1.30
自引率
0.00%
发文量
35
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