Department of Virology, University of Helsinki, Helsinki, Finland.
Center for Virology, Medical University of Vienna, Vienna, Austria.
Transpl Int. 2020 May;33(5):555-566. doi: 10.1111/tri.13584. Epub 2020 Feb 13.
In kidney transplant recipients (KTRs), BK polyomavirus (BKPyV) replication may progress to polyomavirus-associated nephropathy (PVAN). In this retrospective study, we assessed the chemokine CXCL10 in urine and blood samples consecutively acquired from 85 KTRs who displayed different stages of BKPyV replication and eventually developed PVAN. In parallel to progression toward PVAN, CXCL10 gradually increased in blood and urine, from baseline (prior to virus replication) to BKPyV DNAuria (median increase in blood: 42.15 pg/ml, P = 0.0156), from mere DNAuria to low- and high-level BKPyV DNAemia (median increase: 52.60 and 87.26 pg/ml, P = 0.0010 and P = 0.0002, respectively) and peaked with histologically confirmed PVAN (median increase: 145.00 pg/ml, P < 0.0001). CXCL10 blood and urine levels significantly differed among KTRs with respect to simultaneous presence of human cytomegalovirus (P < 0.001) as well as in relation to the clinical severity of respective BKPyV DNAemia episodes (P = 0.0195). CXCL-10 concentrations were particularly lower in KTRs in whom BKPyV DNAemia remained without clinical evidence for PVAN, as compared to individuals who displayed high decoy cell levels, decreased renal function and/or biopsy-proven PVAN (median blood concentration: 266.97 vs. 426.42 pg/ml, P = 0.0282). In conclusion, in KTRs CXCL10 rises in parallel to BKPyV replication and correlates with the gradual development of PVAN.
在肾移植受者(KTRs)中,BK 多瘤病毒(BKPyV)复制可能进展为多瘤病毒相关性肾病(PVAN)。在这项回顾性研究中,我们评估了 85 例 KTR 连续采集的尿液和血液样本中的趋化因子 CXCL10,这些 KTR 显示出不同阶段的 BKPyV 复制,最终发展为 PVAN。随着向 PVAN 的进展,CXCL10 在血液和尿液中逐渐增加,从基线(病毒复制前)到 BKPyV 尿病毒血症(血液中位数增加:42.15pg/ml,P=0.0156),从单纯的尿病毒血症到低水平和高水平 BKPyV 血症(中位数增加:52.60 和 87.26pg/ml,P=0.0010 和 P=0.0002),并在组织学证实的 PVAN 时达到峰值(中位数增加:145.00pg/ml,P<0.0001)。KTR 中,血液和尿液中的 CXCL10 水平在同时存在人巨细胞病毒(P<0.001)以及与各自 BKPyV 血症发作的临床严重程度有关时(P=0.0195)存在显著差异。与显示高诱饵细胞水平、肾功能下降和/或活检证实的 PVAN 的个体相比,BKPyV 血症无临床证据的 KTR 中,CXCL-10 浓度特别低(血液中位数浓度:266.97 与 426.42pg/ml,P=0.0282)。总之,在 KTRs 中,CXCL10 随着 BKPyV 复制而升高,并与 PVAN 的逐渐发展相关。