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汉坦病毒肺综合征患者的肾脏疾病。

Kidney disease in Puumala hantavirus infection.

机构信息

a Faculty of Medicine and Life Sciences , University of Tampere , Tampere , Finland.

b Department of Internal Medicine , Tampere University Hospital , Tampere , Finland.

出版信息

Infect Dis (Lond). 2017 May;49(5):321-332. doi: 10.1080/23744235.2016.1274421. Epub 2017 Jan 3.

DOI:10.1080/23744235.2016.1274421
PMID:28049381
Abstract

Acute kidney injury (AKI) remains a predominant clinical expression of nephropathia epidemica (NE). Its pathogenesis is not yet fully understood. Here, we describe the tissue injury comprehensively and present new data aimed to characterize the injury and explain its pathophysiology. When compared to tubulointerstitial nephritis of a wide variety of other aetiologies, a high degree of proteinuria is a distinguished trait of NE, a finding that is also helpful in the clinical suspicion of the disease. Recently, novel biomarkers for the prediction of severe AKI, including neutrophil gelatinase-associated lipocalin (NGAL), have been identified and ultrastructural tissue changes have been more accurately described. A role for soluble urokinase-type plasminogen activator (suPAR) in the pathogenesis of NE has been suggested, and data on gene polymorphisms, in relation to the severity of AKI have been presented. Smoking is a risk factor for NE and smoking is also associated with aggravated AKI in NE. Although no specific treatment is in sight, recent case reports concerning therapy directed against vascular permeability and vasodilation are of interest. In fact, future work trying to explain the pathophysiology of AKI might need concentrated efforts towards the mechanisms of increased vascular permeability and vasodilatation, which irrespective of organ manifestation, are two major determinants of NE.

摘要

肾综合征出血热(HFRS)仍然是流行性肾病(NE)的主要临床表现。其发病机制尚未完全阐明。在这里,我们全面描述了组织损伤,并提供了旨在表征损伤和解释其病理生理学的新数据。与各种其他病因的肾小管间质性肾炎相比,大量蛋白尿是 NE 的一个显著特征,这一发现也有助于临床怀疑该疾病。最近,已经确定了用于预测严重 AKI 的新型生物标志物,包括中性粒细胞明胶酶相关脂质运载蛋白(NGAL),并且更准确地描述了超微结构组织变化。尿激酶型纤溶酶原激活物(suPAR)在 NE 发病机制中的作用已被提出,并且还提出了与 AKI 严重程度相关的基因多态性的数据。吸烟是 NE 的危险因素,吸烟也与 NE 中 AKI 的加重有关。尽管尚未出现特定的治疗方法,但针对血管通透性和血管舒张的治疗的最近病例报告引起了人们的兴趣。实际上,未来试图解释 AKI 病理生理学的工作可能需要集中精力研究增加血管通透性和血管舒张的机制,这两个机制是 NE 的两个主要决定因素,与器官表现无关。

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