Soleymanian Tayebeh, Rasulzadegan Mohammad Hosein, Sotoodeh Masoud, Ganji Mohammad Reza, Naderi Gholamhosein, Amin Manoochehr, Saddadi Fereshteh, Hakemi Monirsadat, Najafi Iraj
Department of Nephrology Diseases, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Exp Clin Transplant. 2010 Dec;8(4):297-302.
BK virus-associated nephropathy in renal transplant recipients has been increasing in frequency in recent years. This rise is probably because of widespread use of highly potent immunosuppressive regimens, and increased immunosuppression load leads to inability of the recipients to increase a successful antiviral immune response. The incidence of BK virus-associated nephropathy in different reports is between 1% and 10%, with an allograft loss in significant numbers of patients, especially when timely diagnosis and treatment is not restored. We report our experience on BK virus nephropathy in our institute.
All renal transplant biopsies performed at our center between 2001 and 2006 were immunohistochemically screened for the presence of PV-specific protein (SV40 Ag). The histologic diagnosis of BK virus-associated nephropathy was made upon the observation of morphologic changes in tubular epithelium and confirmation with immunohistochemical staining. We reviewed the clinical records of the subjects for demographic, clinical, and laboratory data.
BK virus nephropathy was found in 0.93% of all investigated allograft biopsies (1/108) and in 1.04% of all recipients (1/96; mean age of recipients, 36.48±14.10 years; age range, 13-74 years); 54 of them were male (57%). Type of kidney transplant was living-unrelated donor 76 (79%), living-related donor 13 (14%), and deceased donor 7. Seventeen patients (18%) were transplanted for a second time. Immunosuppressive drugs in 87 of recipients (90%) were cyclosporine, mycophenolate mofetil, and prednisolone. Our patient who developed BK virus-associated nephropathy 9 months after transplant was a 37-year-old man on prednisone, cyclosporine, and azathioprine immunosuppresion. He lost his graft 4 months after diagnosis.
Although BK virus nephropathy after renal transplant is uncommon, it is a serious complication causing loss of the allograft. It should be included in the clinical differential diagnosis of transplant dysfunction.
近年来,肾移植受者中BK病毒相关性肾病的发病率呈上升趋势。这种上升可能是由于强效免疫抑制方案的广泛使用,免疫抑制负荷增加导致受者无法增强成功的抗病毒免疫反应。不同报告中BK病毒相关性肾病的发病率在1%至10%之间,大量患者出现移植肾丢失,尤其是在未及时恢复诊断和治疗的情况下。我们报告了我院在BK病毒肾病方面的经验。
对2001年至2006年在我院进行的所有肾移植活检组织进行免疫组织化学筛查,以检测多瘤病毒特异性蛋白(SV40 Ag)的存在。根据肾小管上皮细胞的形态学变化及免疫组织化学染色结果做出BK病毒相关性肾病的组织学诊断。我们回顾了受试者的临床记录,以获取人口统计学、临床和实验室数据。
在所有调查的移植肾活检组织中,BK病毒肾病的发生率为0.93%(1/108),在所有受者中的发生率为1.04%(1/96;受者平均年龄为36.48±14.10岁;年龄范围为13 - 74岁);其中54例为男性(57%)。肾移植类型为非亲属活体供肾76例(79%),亲属活体供肾13例(14%),尸体供肾7例。17例患者(18%)接受了二次移植。87例受者(90%)使用的免疫抑制药物为环孢素、霉酚酸酯和泼尼松龙。我们的患者在移植9个月后发生BK病毒相关性肾病,为一名37岁男性,接受泼尼松、环孢素和硫唑嘌呤免疫抑制治疗。诊断后4个月移植肾失功。
虽然肾移植后BK病毒肾病并不常见,但它是导致移植肾丢失的严重并发症。应将其纳入移植功能障碍的临床鉴别诊断中。