Hasegawa M, Ito T, Saigo K, Akutsu N, Maruyama M, Otsuki K, Aoyama H, Matsumoto I, Asano T, Kitamura H, Kenmochi T
Department of Surgery, Chiba-East Hospital, National Hospital Organization Chiba, Japan.
Department of Surgery, Chiba-East Hospital, National Hospital Organization Chiba, Japan.
Transplant Proc. 2014;46(2):556-9. doi: 10.1016/j.transproceed.2013.11.114.
BK polyomavirus-associated nephropathy (BKVAN) is an important cause of renal allograft loss. Immunosuppression therapy in renal transplant recipients can lead to the reactivation of latent BK polyomavirus (BKV) infection, leading to BK viruria and viremia. This single-center study aimed to clarify the association between quantitative measurement of BKV DNA and the progression of BKV infection, and secondly to identify the risk factors associated with the evolution of viruria to viremia.
We retrospectively analyzed 266 patients who underwent renal transplantation in our center from October 2006 to February 2013. We examined the viral loads of BKV in urine and plasma by quantitative real-time polymerase chain reaction assay after screening all of the recipients by urinary sediment examination. BKVAN was diagnosed by histological examination with immunohistochemistry of the large T antigen in biopsy specimens.
Overall, 22 recipients showed BK viruria alone, whereas 22 progressed to BK viremia, of which 6 patients were diagnosed with BKVAN. Among BKVAN patients, 2 cases progressed to graft loss at 59 months and 31 months after diagnosis, respectively. In BKVAN group, the plasma viral loads were significantly higher than those in viremia without nephropathy (P < .001). Multivariate analysis revealed that the evolution of viruria to viremia was associated with recipient age over 55 years (odds ratio, 32.08; 95% confidence interval, 2.1-489.5) and tacrolimus exposure (odds ratio, 11.98; 95% confidence interval, 1.34-107.04).
The progression from viremia to BKVAN was strongly associated with increasing plasma viral loads for BKV DNA. The cutoff value of 1 × 10(4) copies/mL for plasma viral loads could differentiate between BKVAN and viremia alone. Further, recipient age over 55 years and tacrolimus exposure were independently associated with the evolution of viruria to viremia.
BK多瘤病毒相关性肾病（BKVAN）是肾移植失败的重要原因。肾移植受者的免疫抑制治疗可导致潜伏的BK多瘤病毒（BKV）感染重新激活，进而导致BK病毒尿症和病毒血症。这项单中心研究旨在阐明BKV DNA定量检测与BKV感染进展之间的关联，其次是确定与病毒尿症发展为病毒血症相关的危险因素。
我们回顾性分析了2006年10月至2013年2月在本中心接受肾移植的266例患者。在对所有受者进行尿沉渣检查筛选后，通过定量实时聚合酶链反应测定法检测尿液和血浆中BKV的病毒载量。通过活检标本中大T抗原的免疫组织化学组织学检查诊断BKVAN。
总体而言，22例受者仅出现BK病毒尿症，而22例进展为BK病毒血症，其中6例患者被诊断为BKVAN。在BKVAN患者中，分别有2例在诊断后59个月和31个月进展为移植失败。在BKVAN组中，血浆病毒载量显著高于无肾病的病毒血症组（P <.001）。多因素分析显示，病毒尿症发展为病毒血症与55岁以上的受者年龄（比值比，32.08；95%置信区间，2.1 - 489.5）和他克莫司暴露（比值比，11.98；95%置信区间，1.34 - 107.04）相关。
从病毒血症进展到BKVAN与BKV DNA血浆病毒载量增加密切相关。血浆病毒载量的临界值为1×10(4)拷贝/mL可区分BKVAN和单纯病毒血症。此外，55岁以上的受者年龄和他克莫司暴露与病毒尿症发展为病毒血症独立相关。
