Current Understanding of Clinical Manifestations of COVID-19 in Glomerular Disease.
Current Understanding of Clinical Manifestations of COVID-19 in Glomerular Disease.
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DOI：
10.1159/000518276
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发表时间：
2021-10
期刊：
影响因子：
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通讯作者：
Mariani L
中科院分区：
文献类型：
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作者：
Shimmel A;Shaikhouni S;Mariani L
新型冠状病毒病（COVID-19），也称为严重急性呼吸道综合征冠状病毒2（SARS-CoV-2），是一种不断演变的大流行病，死亡率很高。关于感染对肾小球疾病患者影响的信息尤其缺乏。了解病毒在肾小球疾病中的作用是不断变化的。这篇综述文章总结了迄今为止发表的关于COVID-19及其在既存和新发肾小球疾病中的表现的数据。虽然患有肾小球疾病的患者由于免疫抑制状态而可能面临更高的严重COVID-19风险，但一些数据表明，少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。有少数病例报告称COVID-19导致患者肾小球疾病复发。已经提出了COVID-19背景下肾损伤、蛋白尿和血尿的多种机制。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肾小管损伤引起的。然而，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，如伊加肾病、抗GBM和ANCA血管炎，这些疾病也在COVID-19患者中有描述。塌陷性肾小球病是HIV相关肾病的标志，在SARS-CoV-2病例中有报道，特别是在携带高危APOL 1等位基因的患者中。由于病毒对ACE 2的亲和力，假设病毒直接侵入肾小球结构导致足细胞病，但这方面的证据仍在研究中。SARS-CoV-2感染可能导致某些患者的肾小球疾病。COVID-19背景下新发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告知临床医生在COVID-19大流行期间对这些患者的管理决策。
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. 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. 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.