Kidney Biopsy Findings in Patients with COVID-19
Kidney Biopsy Findings in Patients with COVID-19
复制标题
DOI：
10.1681/asn.2020060802
复制
发表时间：
2020-09-01
影响因子：
13.6
通讯作者：
D'Agati, Vivette D.
中科院分区：
文献类型：
--
作者：
Kudose, Satoru;Batal, Ibrahim;D'Agati, Vivette D.
冠状病毒病2019 （COVID-19）被认为通过多种机制引起肾损伤。迄今为止，病理分析仅限于患者报告和尸检系列。方法：在2020年3月至6月期间，我们在纽约市的一个中心评估了来自COVID-19患者的原生肾脏和同种异体移植肾脏的活检样本。我们还使用免疫组织化学、原位杂交和电子显微镜检查该组织是否存在严重急性呼吸综合征冠状病毒2 （SARS-CoV-2）。结果研究组纳入17例COVID-19患者（男性12例，黑人12例，中位年龄54岁）。16例患者有合并症，包括高血压、肥胖、糖尿病、恶性肿瘤或肾脏或心脏同种异体移植。9例患者出现COVID-19肺炎。15例患者（88%）出现AKI；9例有肾范围蛋白尿。在14例肾活检患者中，5例诊断为塌陷性肾小球病，1例诊断为微小病变，2例诊断为膜性肾小球病，1例诊断为狼疮性肾炎新月形转化，1例诊断为抗gbm肾炎，4例诊断为孤立性急性肾小管损伤。三个同种异体移植标本显示2A级急性T细胞介导的排斥反应、皮质梗死或急性肾小管损伤。对3例塌陷性肾小球病患者和1例最小改变性肾小球病患者进行基因分型分析，发现4例患者均存在APOL1高危基因变异。我们没有发现肾细胞中存在SARS-CoV-2的明确证据。活检诊断为所有患者的治疗和预后提供了信息。结论COVID-19患者可出现广泛的肾小球和肾小管疾病。我们的研究结果提供了证据，证明肾脏的直接病毒感染是covid -19相关肾损伤的主要病理机制，并涉及细胞因子介导的作用和增强的适应性免疫反应。
Background Coronavirus disease 2019 (COVID-19) is thought to cause kidney injury by a variety of mechanisms. To date, pathologic analyses have been limited to patient reports and autopsy series.Methods We evaluated biopsy samples of native and allograft kidneys from patients with COVID-19 at a single center in New York City between March and June of 2020. We also used immunohistochemistry, in situ hybridization, and electron microscopy to examine this tissue for presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).Results The study group included 17 patients with COVID-19 (12 men, 12 black; median age of 54 years). Sixteen patients had comorbidities, including hypertension, obesity, diabetes, malignancy, or a kidney or heart allograft. Nine patients developed COVID-19 pneumonia. Fifteen patients (88%) presented with AKI; nine had nephrotic-range proteinuria. Among 14 patients with a native kidney biopsy, 5 were diagnosed with collapsing glomerulopathy, 1 was diagnosed with minimal change disease, 2 were diagnosed with membranous glomerulopathy, 1 was diagnosed with crescentic transformation of lupus nephritis, 1 was diagnosed with anti-GBM nephritis, and 4 were diagnosed with isolated acute tubular injury. The three allograft specimens showed grade 2A acute T cell-mediated rejection, cortical infarction, or acute tubular injury. Genotyping of three patients with collapsing glomerulopathy and the patient with minimal change disease revealed that all four patients had APOL1 high-risk gene variants. We found no definitive evidence of SARS-CoV-2 in kidney cells. Biopsy diagnosis informed treatment and prognosis in all patients.Conclusions Patients with COVID-19 develop a wide spectrum of glomerular and tubular diseases. Our findings provide evidence against direct viral infection of the kidneys as the major pathomechanism for COVID-19-related kidney injury and implicate cytokine-mediated effects and heightened adaptive immune responses.