Current Understanding of Clinical Manifestations of COVID-19 in Glomerular Disease.

Allison Shimmel, Salma Shaikhouni, Laura Mariani
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引用次数: 5

Abstract

Background: The novel coronavirus disease (COVID-19), also known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is an evolving pandemic with significant mortality. Information about the impact of infection on glomerular disease patients in particular has been lacking. Understanding the virus's effect in glomerular disease is constantly changing. This review article summarizes the data published thus far on COVID-19 and its manifestations in pre-existing and de novo glomerular disease.

Summary: While patients with glomerular disease may be at higher risk of severe COVID-19 due to their immunosuppressed status, some data suggest that a low amount of immunosuppression may be helpful in mitigating the systemic inflammatory response which is associated with high mortality rates in COVID-19. There have been a few case reports on COVID-19 causing glomerular disease relapse in patients. Multiple mechanisms have been proposed for kidney injury, proteinuria, and hematuria in the setting of COVID-19. More commonly, these are caused by direct tubular injury due to hemodynamic instability and hypoxic injury. However, the cytokine storm induced by COVID-19 may trigger common post-viral glomerular disease such as IgA nephropathy, anti-GBM, and ANCA vasculitis that have also been described in COVID-19 patients. Collapsing glomerulopathy, a hallmark of HIV-associated nephropathy, is being reported SARS-CoV-2 cases, particularly in patients with high-risk APOL1 alleles. Direct viral invasion of glomerular structures is hypothesized to cause a podocytopathy due to virus's affinity to ACE2, but evidence for this remains under study.

Key messages: Infection with SARS-CoV-2 may cause glomerular disease in certain patients. The mechanism of de novo glomerular disease in the setting of COVID-19 is under study. The management of patients with existing glomerular disease poses unique challenges, especially with regard to immunosuppression management. Further studies are needed to inform clinician decisions about the management of these patients during the COVID-19 pandemic.

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COVID-19在肾小球疾病中的临床表现
背景:新型冠状病毒病(COVID-19),也称为严重急性呼吸综合征冠状病毒2 (SARS-CoV-2),是一种不断演变的大流行,死亡率很高。特别是关于感染对肾小球疾病患者影响的信息一直缺乏。对这种病毒在肾小球疾病中的作用的认识在不断变化。本文综述了迄今为止发表的关于COVID-19及其在既往肾小球疾病和新生肾小球疾病中的表现的资料。摘要:肾小球疾病患者由于其免疫抑制状态可能具有更高的严重COVID-19风险,但一些数据表明,低剂量的免疫抑制可能有助于减轻与COVID-19高死亡率相关的全身炎症反应。COVID-19引起肾小球疾病患者复发的病例报道不多。在COVID-19的背景下,肾损伤、蛋白尿和血尿的多种机制已经被提出。更常见的是,这些是由血流动力学不稳定和缺氧损伤引起的直接小管损伤引起的。然而,由COVID-19诱导的细胞因子风暴可能引发常见的病毒后肾小球疾病,如IgA肾病、抗gbm和ANCA血管炎,这些也在COVID-19患者中被描述。塌陷性肾小球病变是艾滋病毒相关肾病的标志,正在报告SARS-CoV-2病例,特别是在高风险APOL1等位基因患者中。由于病毒对ACE2的亲和力,假设病毒直接侵入肾小球结构可引起足细胞病,但这方面的证据仍在研究中。关键信息:SARS-CoV-2感染可能导致某些患者肾小球疾病。COVID-19背景下新生肾小球疾病的机制正在研究中。现有肾小球疾病患者的管理提出了独特的挑战,特别是在免疫抑制管理方面。需要进一步的研究来为临床医生在COVID-19大流行期间对这些患者的管理提供信息。
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