Dobrava汉坦病毒和合并SARS-CoV-2感染,模拟血栓性微血管病变,并对单剂量Eculizumab有反应

NDT Plus Pub Date : 2023-09-27 DOI:10.1093/ckj/sfad222
Simon Aberger, Nicolas Kozakowski, Zoltán Proházka, Thomas Pleininger, Hermann Salmhofer
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引用次数: 0

摘要

当前的严重急性呼吸综合征冠状病毒2 (SARS-CoV-2)大流行重新将科学兴趣集中在了解全身性病毒性疾病的病理生理学上。补体激活被认为是急性呼吸窘迫综合征和汉坦病毒出血热伴肾综合征中内皮损伤和微血管血栓形成的驱动因素。在这种情况下,我们希望报告一例严重汉坦病毒病,同时伴有模拟血栓性微血管病的SARS-CoV-2感染,炎症标志物、血液学参数和蛋白尿对eculizumab的快速反应。这些发现支持病毒相关内皮损伤的疾病模型,涉及替代途径补体激活。在危及生命的病毒性疾病中,是否可以通过补体抑制来减轻终末器官损伤需要进一步的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dobrava hantavirus and coinciding SARS-CoV-2 infection mimicking thrombotic microangiopathy and responding to a single dose of Eculizumab
ABSTRACT The current severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has refocused scientific interest on gaining insight into the pathophysiology of systemic viral diseases. Complement activation has been characterized as a driver of endothelial injury and microvascular thrombosis in acute respiratory distress syndrome as well as hantavirus hemorrhagic fever with renal syndrome. On this occasion, we wish to report a case of severe hantavirus disease with coinciding SARS-CoV-2 infection mimicking thrombotic microangiopathy with rapid response of inflammatory markers, hematologic parameters and proteinuria to eculizumab. These findings support a disease model of virus-associated endothelial injury involving alternative pathway complement activation. Future studies are needed to explore whether end organ damage can be mitigated by complement inhibition in life-threatening viral disease.
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