Lipshutz G S, Mahanty H, Feng S, Hirose R, Stock P G, Kang S-M, Freise C E
Department of Surgery, University of California, San Francisco, 94143, USA.
Transplant Proc. 2004 May;36(4):1097-8. doi: 10.1016/j.transproceed.2004.04.039.
With the introduction of more potent immunosuppressive agents, rejection rates have decreased markedly in simultaneous pancreas-kidney transplant (SPK) recipients. However, with more intense immunosuppression, opportunistic infections such as polyoma virus have been more frequent. The purpose of this article is to outline the clinical course of SPK patients who developed documented polyoma infection in the transplanted kidney.
A retrospective review of 146 consecutive SPK recipients from 1996 to 2002 was performed. Induction and maintenance immunosuppression, surgical complications, rejection episodes, and opportunistic infections were reviewed. Patients who developed biopsy-proven polyoma virus infection in the renal allograft were identified.
Nine patients (6%) were identified who developed polyoma. All had received induction therapy with either OKT3 (5 mg/d for 10.5 days) or thymoglobulin (5.7 mg/kg). Patients without polyoma had received similar induction. Maintenance immunosuppression included Prograf/MMF in six patients, CsA/MMF in two, and CsA/azathioprine in one. Time to diagnosis was an average of 359.3 days (range 136 to 836) after transplantation. Two patients had undergone treatment for kidney rejection prior to the diagnosis of polyoma. Immunosuppression was decreased in all patients when polyoma was identified, and more recently Cidofovir has been administered. Despite these interventions, five of the nine lost kidney function (creatinine > 5.0 or resumption of dialysis). However, none of the nine developed pancreatic abnormalities as demonstrated by normal blood glucose and amylase and no requirement for exogenous insulin. Two patients underwent LRRT more than 1 year after polyoma diagnosis; both have normal kidney function (Cr < 1.5 mg/dL) at 4 years of follow-up. Polyoma virus was the leading cause of renal loss in this cohort of patients.
Polyoma is a serious concern for SPK transplant recipients. The pancreas, however, is spared from clinical evidence of infection, and no rejection was noted when immunosuppression was decreased. These graft losses appear to be a penalty of more potent immunosuppression, and a better treatment strategy is needed to prevent renal graft loss when polyoma is diagnosed. Retransplantation can be considered based on our limited experience.
随着更强效免疫抑制剂的应用,胰肾联合移植(SPK)受者的排斥反应发生率显著下降。然而,随着免疫抑制强度的增加,多瘤病毒等机会性感染更为常见。本文旨在概述移植肾发生确诊多瘤病毒感染的SPK患者的临床病程。
对1996年至2002年连续146例SPK受者进行回顾性研究。回顾诱导和维持免疫抑制、手术并发症、排斥反应发作及机会性感染情况。确定肾移植活检证实发生多瘤病毒感染的患者。
9例(6%)患者发生多瘤病毒感染。所有患者均接受过OKT3(5mg/d,共10.5天)或抗胸腺细胞球蛋白(5.7mg/kg)诱导治疗。未发生多瘤病毒感染的患者接受过类似诱导治疗。维持免疫抑制方案中,6例患者采用普乐可复/霉酚酸酯,2例采用环孢素/霉酚酸酯,1例采用环孢素/硫唑嘌呤。诊断时间平均为移植后359.3天(范围136至836天)。2例患者在多瘤病毒诊断前曾接受过肾排斥反应治疗。确诊多瘤病毒感染后,所有患者免疫抑制均减量,近期开始应用西多福韦。尽管采取了这些干预措施,9例患者中有5例肾功能丧失(肌酐>5.0或恢复透析)。然而,9例患者均未出现胰腺异常,血糖和淀粉酶正常,无需外源性胰岛素治疗。2例患者在多瘤病毒诊断1年多后接受了再次肾移植;随访4年时,二者肾功能均正常(肌酐<1.5mg/dL)。多瘤病毒是该组患者肾丢失的主要原因。
多瘤病毒是SPK移植受者的严重问题。然而,胰腺未出现感染的临床证据,免疫抑制减量时未观察到排斥反应。这些移植肾丢失似乎是更强效免疫抑制的代价,诊断多瘤病毒感染时需要更好的治疗策略以防止肾移植丢失。根据我们有限的经验可考虑再次移植。