J Korean Soc Transplant.
2002 Dec;16(2):219-226.
BK Virus Induced Interstitial Nephritis in Renal Transplants: Diagnosis, Treatment and Prognosis
- Affiliations
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- 1Department of Surgery, Yonsei University College of Medicine, Seoul, Korea. yukim@yumc.yonsei.ac.kr
- 2Department of Pathology, Yonsei University College of Medicine, Seoul, Korea.
- 3Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
- 4Department of Laboratory Medicine, Yonsei University College of Medicine, Seoul, Korea.
- 5Seoul Adventist Hospital, Seoul, Korea.
Abstract
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PURPOSE: It is difficult to differentiate BKV nephritis (BKVN) from acute rejection. We diagnosed 8 cases of BKVN in renal transplantation recipients. Herein, we report the clinical nature of BKVN in terms of diagnosis, treatment and prognosis.
METHODS
Between June 1998 and September 2002, 8 cases of BKVN were confirmed by H and E stain, immunohistochemical study against SV40, and electron microscopy in renal allograft biopsy samples. Additionally, between April and September 2002, we obtained urine sample for urine cytology from 49 potential donors, 40 end-stage renal failure patients awaiting renal transplantation, and 140 renal transplant recipients who were hospitalized with variable causes and 32 renal transplants as a routine follow-up.
RESULTS
In 7 male and 1 female patients, BKVN was diagnosed mean of 20.4 months after transplantation. The kind of immunosuppression they had been on were mycophenolate mofetil (6/8), azathioprine (1/8), cyclosporin (4/8), tacrolimus (4/8). Range of whole blood levels of cyclosporine and tacrolimus at the time of diagnosis of BKVN were 187.5~252.5 ng/ml and 11~16.5 ng/ml, respectively. Four patients had treated acute rejection episode, and in 6 patients, pathologically proven acute rejection was found concomitantly with BKVN. After reduction of net immunosuppression (discontinuation of MMF and AZA, dose reduction of cyclosporine or tacrolimus, and switch from tacrolimus to cyclosporine), renal function of 3 patients was fully recovered. However, 4 patients with delayed diagnosis lost grafts. In urine cytologic examination, 15 patients (one in end-stage renal failure patient, 10 in renal transplant recipients with elevated serum creatinine, 2 in patients with other infection, and 2 in other situation) were found to secrete decoy cell through urine.
CONCLUSION
BKVN should be considered in the differential diagnosis of renal allograft dysfunction. Early diagnosis of BKVN and reduction of net immunosuppression can rescue the grafts. Monitoring of decoy cell in the urine cytology is a simple diagnostic tool both for screening of graft with dysfunction and follow-up of grafts after diagnosis and treatment of BKVN.