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BK 多瘤病毒在实体器官移植中的作用。

BK polyomavirus in solid organ transplantation.

机构信息

Infectious Diseases and Hospital Epidemiology, University Hospital Basel, Basel, Switzerland.

出版信息

Am J Transplant. 2013 Mar;13 Suppl 4:179-88. doi: 10.1111/ajt.12110.

DOI:10.1111/ajt.12110
PMID:23465010
Abstract

The human BK polyomavirus (BKV) is the major cause of polyomavirus-associated nephropathy (PyVAN) putting 1-15% of kidney transplant patients at risk of premature allograft failure, but is less common in other solid organ transplants. Because effective antiviral therapies are lacking, screening kidney transplant patients for BKV replication in urine and blood has become the key recommendation to guide the reduction of immunosuppression in patients with BKV viremia. This intervention allows for expanding BKV-specific cellular immune responses, curtailing of BKV replication in the graft, and clearance of BKV viremia in 70-90% patients. Postintervention rejection episodes occur in 8-12%, most of which are corticosteroid responsive. Late diagnosis is faced with irreversible functional decline, poor treatment response, and graft loss. Adjunct therapies such as cidofovir, leflunomide and intravenous immunoglobulins have been used, but the benefit is not documented in trials. Retransplantation after PyVAN is largely successful, but requires close monitoring for recurrent BKV viremia.

摘要

人类 BK 多瘤病毒(BKV)是多瘤病毒相关性肾病(PyVAN)的主要病因,使 1-15%的肾移植患者面临移植肾功能丧失的风险,而在其他实体器官移植中则较少见。由于缺乏有效的抗病毒治疗方法,因此对肾移植患者的尿液和血液中的 BKV 复制情况进行筛查,已成为指导减少 BKV 血症患者免疫抑制的关键建议。这种干预措施可以扩大 BKV 特异性细胞免疫反应,抑制移植肾中的 BKV 复制,并使 70-90%的患者清除 BKV 血症。干预后发生排斥反应的概率为 8-12%,其中大多数对皮质类固醇治疗有反应。晚期诊断则面临肾功能不可逆转的下降、治疗反应不佳和移植物丢失的风险。已使用过辅助治疗方法,如更昔洛韦、来氟米特和静脉注射免疫球蛋白,但临床试验并未证明这些方法有益。PyVAN 后再次移植的成功率较高,但需要密切监测复发性 BKV 血症。

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