Shimmel Allison, Shaikhouni Salma, Mariani Laura
College of Medicine and Life Sciences, University of Toledo, Toledo, Ohio, USA.
Department of Nephrology, Michigan Medicine, Ann Arbor, Michigan, USA.
Glomerular Dis. 2021 Jul 8;1(4):250-264. doi: 10.1159/000518276. eCollection 2021 Oct.
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.
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病,具有很高的死亡率。尤其缺乏关于感染对肾小球疾病患者影响的信息。对该病毒在肾小球疾病中的作用的认识也在不断变化。这篇综述文章总结了迄今为止发表的关于COVID-19及其在既往存在的和新发的肾小球疾病中的表现的数据。
虽然肾小球疾病患者因其免疫抑制状态可能面临更高的发生严重COVID-19的风险,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。已有一些关于COVID-19导致患者肾小球疾病复发的病例报告。针对COVID-19背景下的肾损伤、蛋白尿和血尿,人们提出了多种机制。更常见的是,这些是由血流动力学不稳定和缺氧损伤导致的直接肾小管损伤引起的。然而,COVID-19引发的细胞因子风暴可能会触发常见的病毒后肾小球疾病,如IgA肾病、抗肾小球基底膜病和ANCA血管炎,这些在COVID-19患者中也有描述。正在SARS-CoV-2病例中报告塌陷性肾小球病,这是HIV相关肾病的一个标志,特别是在具有高危APOL1等位基因的患者中。据推测,病毒对肾小球结构的直接侵袭会因病毒对ACE2的亲和力而导致足细胞病,但这方面的证据仍在研究中。
SARS-CoV-2感染可能在某些患者中导致肾小球疾病。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带来了独特的挑战,特别是在免疫抑制管理方面。需要进一步研究,为临床医生在COVID-19大流行期间管理这些患者的决策提供依据。