DiscussionTo the best of our knowle

DiscussionTo the best of our knowledge, this is the first description of the pathological featuresof renal injury in the setting of COVID-19 outside autopsies series. The most striking findingin our patient was the collapsing FSGS. This finding suggests that FSGS could account for theheavy proteinuria reported in a significant proportion of patients with COVID-191. Thecollapsing FSGS is a known complication of other viral infections, in particular the humanimmunodeficiency virus (HIV)4, but also the cytomegalovirus5 and the parvovirus B196. ForHIV a direct toxic viral effect on podocytes has been documented7. The receptor for SARSCoV-2, membrane-bound angiotensin-converting enzyme 2 (ACE2), is expressed onpodocytes8,9. PCR for SARS-CoV-2 was negative in kidney biopsy samples, but the techniquehas a notoriously low rate of detection in non-respiratory samples (including blood andurine)10 and the quality of the extracted RNA material was poor. However, in our patient’scase, the presence of viral particles in the podocytes, revealed by electron microscopy study,strongly suggests a direct toxic viral effect on podocytes.Collapsing FSGS, with or without acute tubular necrosis, can also complicate thecourse of hemophagocytic syndrome11, a disorder characterized by an increased release of awide range of cytokines. In our patient, normal levels of cytokines, in particular IL6, whilstinflammation markers were still increased, plead against this hypothesis. However, a potentialvirus-driven intra-renal cytokines release cannot be excluded.Besides, since our patient is of African origin, it cannot be excluded that APOL1variant may have contributed to the pathogenesis of collapsing FSGS, since APOL1 is arecognized risk factor for the development collapsing FSGS in HIV and non-HIV patients4.In our patient, acute tubular necrosis developed in the absence of hemodynamiccompromise or severe pulmonary involvement. This suggests that tubular injury in COVID-19 patients, unlike that seen in coronavirus-associated severe acute respiratory syndrome(SARS)12, is not predominantly ischemic. The possible underlying mechanisms are a directviral toxicity on tubular cells that also harbour ACE2 or a cytokine-mediated tubular damage.In addition, the initial heavy proteinuria in our patient may have also contributed to tubularnecrosis.Overall, in contrast to lung injury, kidney injury in COVID-19 does not appear toinclude a predominant inflammatory component. This observation suggests that collapsingFSGS, potentially resulting from a direct viral effect on podocytes, probably belongs to thespectrum of COVID-19-associated renal involvement.

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结果 (简体中文) 1: [复制]

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讨论 就我们所知，这是首次 在尸检系列之外的COVID-19背景下描述肾脏损伤的病理特征。 在我们的患者中最惊人的发现是崩溃的FSGS。这一发现表明，FSGS可以解释 COVID-191患者中报告的大量蛋白尿。所述 折叠FSGS是其他病毒感染的已知的并发症，特别是人 免疫缺陷病毒（HIV）4，而且还cytomegalovirus5和细小病毒B196。对于 HIV，已经证明对足细胞有直接毒性病毒作用7。 膜结合的血管紧张素转换酶2（ACE2）的SARSCoV -2 受体表达于 足细胞8,9。肾活检样品中SARS-CoV-2的PCR阴性，但是该技术 在非呼吸性样品（包括血液和 尿液）中的检出率极低，10且提取的RNA物质质量差。但是，就我们的患者 而言，通过电子显微镜研究发现，足细胞中存在病毒颗粒， 强烈暗示了对足细胞有直接的毒性病毒作用。 伴有或不伴有急性肾小管坏死的FSGS塌陷也会使 噬血细胞综合症的病情复杂化11 ，该病的特征是 多种细胞因子释放增加。在我们的患者中，细胞因子，特别是IL6的正常水平，而 炎症标志物仍在增加，反对这一假说。但是， 不能排除潜在的病毒驱动的肾内细胞因子释放。 此外，由于我们的患者是非洲血统，因此不能排除APOL1 变异可能是导致FSGS崩溃的原因，因为APOL1是 公认的导致HIV和非HIV患者崩溃FSGS的危险因素。 在我们的患者中，在没有血流动力学 损害或严重的肺部受累的情况下发生了急性肾小管坏死。这表明 与冠状病毒相关的严重急性呼吸系统综合症不同，COVID- 19患者的肾小管损伤 （SARS）12，不是局部缺血。可能的潜在机制是 对也带有ACE2或细胞因子介导的肾小管损害的肾小管细胞的直接病毒毒性。 此外，我们患者最初的重蛋白尿也可能导致了肾小管 坏死。 总体而言，与肺损伤相反，COVID-19中的肾损伤似乎不 包括主要的炎症成分。该观察结果表明 ，可能由于对足细胞的直接病毒作用而导致的塌陷的FSGS可能属于与 COVID-19相关的肾脏受累范围。

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结果 (简体中文) 2:[复制]

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Discussion To the best of our knowledge, this is the first description of the pathological features of renal injury in the setting of COVID-19 outside autopsies series. The most striking finding in our patient was the collapsing FSGS. This finding suggests that FSGS could account for the heavy proteinuria reported in a significant proportion of patients with COVID-191. The collapsing FSGS is a known complication of other viral infections, in particular the human immunodeficiency virus (HIV)4, but also the cytomegalovirus5 and the parvovirus B196. For HIV a direct toxic viral effect on podocytes has been documented7. The receptor for SARSCoV- 2, membrane-bound angiotensin-converting enzyme 2 (ACE2), is expressed on podocytes8,9. PCR for SARS-CoV-2 was negative in kidney biopsy samples, but the technique has a notoriously low rate of detection in non-respiratory samples (including blood and urine)10 and the quality of the extracted RNA material was poor. However, in our patient’s case, the presence of viral particles in the podocytes, revealed by electron microscopy study, strongly suggests a direct toxic viral effect on podocytes. Collapsing FSGS, with or without acute tubular necrosis, can also complicate the course of hemophagocytic syndrome11, a disorder characterized by an increased release of a wide range of cytokines. In our patient, normal levels of cytokines, in particular IL6, whilst inflammation markers were still increased, plead against this hypothesis. However, a potential virus-driven intra-renal cytokines release cannot be excluded. Besides, since our patient is of African origin, it cannot be excluded that APOL1 variant may have contributed to the pathogenesis of collapsing FSGS, since APOL1 is a recognized risk factor for the development collapsing FSGS in HIV and non-HIV patients4. In our patient, acute tubular necrosis developed in the absence of hemodynamic compromise or severe pulmonary involvement. This suggests that tubular injury in COVID- 19 patients, unlike that seen in coronavirus-associated severe acute respiratory syndrome (SARS)12, is not predominantly ischemic. The possible underlying mechanisms are a direct viral toxicity on tubular cells that also harbour ACE2 or a cytokine-mediated tubular damage. In addition, the initial heavy proteinuria in our patient may have also contributed to tubular necrosis. Overall, in contrast to lung injury, kidney injury in COVID-19 does not appear to include a predominant inflammatory component. This observation suggests that collapsing FSGS, potentially resulting from a direct viral effect on podocytes, probably belongs to the spectrum of COVID-19-associated renal involvement.

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结果 (简体中文) 3:[复制]

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讨论 据我们所知，这是病理特征的第一次描述 在COVID-19体外系列尸检中的肾损伤。最惊人的发现 在我们的病人身上是崩溃的fsg。这一发现表明FSGS可以解释 有相当比例的COVID-191患者出现严重蛋白尿。这个 FSGS崩溃是其他病毒感染的已知并发症，特别是人类 免疫缺陷病毒（HIV）4，也有巨细胞病毒5和细小病毒B196。为了 HIV是一种对足细胞有直接毒性的病毒。SARSCoV受体- 2，膜结合血管紧张素转换酶2（ACE2），表达于 足细胞8,9。肾活检标本中SARS-CoV-2的聚合酶链反应为阴性，但是 在非呼吸性样本（包括血液和 尿）10和提取的RNA材料质量差。但是，在我们病人的 例，足细胞中病毒颗粒的存在，通过电子显微镜研究发现， 强烈提示病毒对足细胞有直接毒性作用。 塌陷性FSGS，伴有或不伴有急性肾小管坏死，也可使 噬血细胞综合征病程11，一种以血细胞释放增加为特征的疾病 广泛的细胞因子。在我们的病人中，细胞因子水平正常，特别是IL6，同时 炎症标记物仍在增加，反驳了这一假设。然而，一个潜在的 不能排除病毒驱动的肾内细胞因子释放。 此外，由于我们的病人来自非洲，不能排除APOL1 变异体可能是导致FSGS塌陷的原因之一，因为APOL1是一种 HIV和非HIV患者中发生FSG崩溃的公认风险因素4。 在我们的病人中，急性肾小管坏死是在没有血流动力学的情况下发生的 折衷或严重肺部受累。这表明COVID的肾小管损伤- 19名患者，与冠状病毒相关的严重急性呼吸综合征不同 （SARS）12，主要不是缺血。可能的潜在机制是 病毒对同样含有ACE2或细胞因子介导的肾小管损伤的肾小管细胞的毒性。 此外，我们病人最初的严重蛋白尿也可能导致肾小管 坏死。 总的来说，与肺损伤相比，COVID-19的肾损伤似乎没有 包括主要的炎症成分。这个观察结果表明 FSGS可能是由病毒对足细胞的直接作用引起的，可能属于 COVID-19相关肾损害的频谱。

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