一名冠状病毒病 2019(COVID-19)患者的膜性肾病:病例报告。

Clinical Nephrology. Case Studies Pub Date : 2021-02-19 eCollection Date: 2021-01-01 DOI:10.5414/CNCS110379
Jing Miao, Mary E Fidler, Samih H Nasr, Christopher P Larsen, Ziad M Zoghby
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摘要

导言:虽然呼吸系统、免疫系统和凝血系统是冠状病毒疾病 2019(COVID-19)的主要攻击目标,但肾功能障碍也很常见,表现为急性肾损伤(AKI)。COVID-19 中的大多数急性肾损伤病例表现为急性肾小管损伤(ATI),同时伴有多器官功能衰竭。虽然最初的肾脏病理结果仅限于急性肾小管坏死和塌陷性肾小球病变,但最近的一个病例系列报告了更多的病理结果:在此,我们报告了一例膜性肾病(MN)病例,患者是一名 81 岁的西班牙裔男性,基础慢性肾病(CKD)3 期,在 COVID-19 的背景下发生了 ATI。患者因缺氧性呼吸衰竭住院,AKI 3 期,SARS-CoV-2 阳性筛查 6 天后血清肌酐为 7.1 mg/dL。他被发现有肾病范围蛋白尿、糖尿(血清葡萄糖正常)、贫血和低白蛋白血症。肾活检显示有 ATI 和早期 MN。原发性和继发性 MN 的检查结果均未显示,血清 PLA2R 抗体呈阴性。荚膜细胞中未观察到病毒颗粒:结论:尽管MN可能是偶然发生的,但这一观察结果提出了一个问题:SARS-CoV-2感染是否会诱发或加重与COVID-19相关的免疫反应异常引起的潜在MN。
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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Membranous nephropathy in a patient with coronavirus disease 2019 (COVID-19): A case report.

Introduction: Though respiratory, immune, and coagulation systems are major targets of coronavirus disease 2019 (COVID-19), kidney dysfunction, presenting with acute kidney injury (AKI), is also common. Most AKI cases in COVID-19 manifest as acute tubular injury (ATI) in conjunction with multiorgan failure. While initial renal pathological findings were limited to acute tubular necrosis and collapsing glomerulopathy, a recent case series reported a larger spectrum of findings.

Case report: Here, we report a case of membranous nephropathy (MN) in an 81-year-old Hispanic man with underlying chronic kidney disease (CKD) stage 3 who developed ATI in the setting of COVID-19. The patient was hospitalized for hypoxic respiratory failure in the setting of AKI stage 3 with serum creatinine 7.1 mg/dL 6 days after a positive-SARS-CoV-2 screening. He was found to have nephrotic range proteinuria, glycosuria (with normal serum glucose), anemia, and hypoalbuminemia. Kidney biopsy showed ATI and early MN. Workup for primary and secondary MN was unrevealing, and serum PLA2R antibody was negative. No viral particles were observed in podocytes.

Conclusion: Although the MN could be incidental, this observation raises the question of whether SARS-CoV-2 infection can trigger or worsen an underlying MN from an exaggerated immune response associated with COVID-19.

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