Schachtner Thomas, Babel Nina, Reinke Petra
Department of Nephrology and Internal Intensive Care, Charité University Medicine Berlin, Berlin, Germany.
Berlin-Brandenburg Center of Regenerative Therapies (BCRT), Berlin, Germany.
Transpl Int. 2015 Sep;28(9):1081-91. doi: 10.1111/tri.12601. Epub 2015 May 22.
Two of three reactivations of latent BKV-infection occur within the first 6 months after renal transplantation. However, a clear differentiation between early-onset and late-onset BKV-replication is lacking. Here, we studied all kidney transplant recipients (KTRs) at our single transplant center between 2004 and 2012. A total of 103 of 862 KTRs were diagnosed with BK viremia (11.9%), among which 24 KTRs (2.8%) showed progression to BKV-associated nephropathy (BKVN). Sixty-seven KTRs with early-onset BKV-replication (65%) and 36 KTRs with late-onset BKV-replication (35%) were identified. A control group of 598 KTRs without BKV-replication was used for comparison. Lymphocyte-depleting induction, CMV-reactivation, and acute rejection increased the risk of early-onset BKV-replication (P < 0.05). Presensitized KTRs undergoing renal retransplantation were those at increased risk of late-onset BKV-replication (P < 0.05). Among KTRs with BK viremia, higher doses of mycophenolate increased the risk of progression to BKVN (P = 0.004). KTRs with progression to BKVN showed inferior allograft function (P < 0.05). KTRs with late-onset BK viremia were more likely not to recover to baseline creatinine after BKV-replication (P = 0.018). Our data suggest different risk factors in the pathogenesis of early-onset and late-onset BKV-reactivation. While a more intensified immunosuppression is associated with early-onset BKV-replication, a chronic inflammatory state in presensitized KTRs may contribute to late-onset BKV-replication.
潜伏性BK病毒感染的三次再激活事件中有两次发生在肾移植后的头6个月内。然而，目前尚缺乏对早发性和迟发性BK病毒复制的明确区分。在此，我们研究了2004年至2012年间在我们单一移植中心的所有肾移植受者（KTR）。862名KTR中共有103名被诊断为BK病毒血症（11.9%），其中24名KTR（2.8%）进展为BK病毒相关性肾病（BKVN）。确定了67名早发性BK病毒复制的KTR（65%）和36名迟发性BK病毒复制的KTR（35%）。使用598名无BK病毒复制的KTR作为对照组进行比较。淋巴细胞清除诱导、巨细胞病毒再激活和急性排斥增加了早发性BK病毒复制的风险（P<0.05）。接受肾再次移植的致敏KTR是迟发性BK病毒复制风险增加的人群（P<0.05）。在患有BK病毒血症的KTR中，更高剂量的霉酚酸增加了进展为BKVN的风险（P=0.004）。进展为BKVN的KTR显示移植肾功能较差（P<0.05）。迟发性BK病毒血症的KTR在BK病毒复制后更有可能无法恢复到基线肌酐水平（P=0.018）。我们的数据表明，早发性和迟发性BK病毒再激活的发病机制中存在不同的危险因素。虽然更强的免疫抑制与早发性BK病毒复制有关，但致敏KTR中的慢性炎症状态可能导致迟发性BK病毒复制。
