Hayat Ashik, Mukhopadhyay Ratna, Radhika Srinivasan, Sachdeva Manupdesh S, Nada Ritambhra, Joshi Kusum, Sakhuja Vinay, Jha Vivekanand
Department of Nephrology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Nephrology (Carlton). 2008 Apr;13(2):157-63. doi: 10.1111/j.1440-1797.2007.00861.x.
BK polyoma virus (BKV) has emerged as an important cause of acute and chronic allograft injury in renal transplant recipients. Reactivation of latent infection requires reduction in cell-mediated immunity. We hypothesized that BKV could get reactivated in the urinary tract of patients with end-stage renal disease (ESRD) and impact the allograft function after these individuals undergo transplantation.
We prospectively examined the urine specimens of 68 ESRD patients and their donors for BKV inclusion containing decoy cells with Papanicoulau staining and immunohistochemistry. Polymerase chain reaction was carried out to confirm the presence of viral DNA. Urine examination was repeated 3-9 months after transplantation and during episodes of graft dysfunction. All graft dysfunction episodes were investigated by biopsy. BKV-associated nephropathy was confirmed by immunoperoxidase staining. Graft loss and doubling of serum creatinine were the study end-points.
Decoy cells were detected in 22 ESRD patients and four donors (P < 0.0001). All 22 continued decoy cell excretion after transplantation and two fresh excreters were noted. Patients exhibiting decoy cells had more frequent graft dysfunction episodes (67% vs 30%, P = 0.003) and higher serum creatinine value (P < 0.001). About 33% patients achieved the combined end-points in the BK viruria group, compared with 11% in the non-decoy cell excreters (P = 0.03). Histologically proved BKV nephropathy was noted in 7% cases; all decoy cell excreters.
We conclude that reactivation of latent BKV infection can occur in ESRD and confers an increased risk of graft dysfunction after transplantation. The mechanism of graft dysfunction in decoy cell excreters who do not develop overt nephropathy needs more studies.
BK 多瘤病毒（BKV）已成为肾移植受者急性和慢性移植肾损伤的重要原因。潜伏感染的重新激活需要细胞介导的免疫功能降低。我们推测，终末期肾病（ESRD）患者的泌尿道中 BKV 可能重新激活，并在这些个体接受移植后影响移植肾功能。
我们前瞻性地检查了 68 例 ESRD 患者及其供体的尿液标本，通过巴氏染色和免疫组织化学检测含 BKV 包涵体的诱饵细胞。进行聚合酶链反应以确认病毒 DNA 的存在。移植后 3 - 9 个月以及移植肾功能障碍发作期间重复进行尿液检查。所有移植肾功能障碍发作均通过活检进行调查。通过免疫过氧化物酶染色确诊 BKV 相关性肾病。移植肾丢失和血清肌酐翻倍是研究终点。
在 22 例 ESRD 患者和 4 例供体中检测到诱饵细胞（P < 0.0001）。所有 22 例患者在移植后持续排出诱饵细胞，并且发现了 2 例新的排出者。出现诱饵细胞的患者移植肾功能障碍发作更频繁（67% 对 30%，P = 0.003），血清肌酐值更高（P < 0.001）。BK 病毒尿组中约 33% 的患者达到联合终点，而非诱饵细胞排出者中为 11%（P = 0.03）。组织学证实的 BKV 肾病在 7% 的病例中被发现；所有病例均为诱饵细胞排出者。
我们得出结论，ESRD 患者中潜伏的 BKV 感染可重新激活，并在移植后增加移植肾功能障碍的风险。未发生明显肾病的诱饵细胞排出者中移植肾功能障碍的机制需要更多研究。
