Journal List > J Korean Soc Transplant > v.26(1) > 1034378

Yoo, Park, Oh, Chae, and Lee: Clinical Manifestations of BK Virus Infection in Kidney Transplant Recipients: A Single Center Experience

Abstract

Background

BK virus (BKV) has emerged as an important cause of graft dysfunction and failure in renal transplant recipients. Reduction of immunosuppressive therapy is accepted as the primary strategy for management of BKV infection in renal transplant recipients, a strategy which frequently results in graft dysfunction and failure. Herein, a single center experience of BKV infection in renal transplant recipients is presented with an emphasis on the management of BKV infection.

Methods

We retrospectively reviewed the medical records of 107 renal transplant recipients who were treated at the outpatient clinic in Seoul National University Bundang Hospital from April 2003 to April 2011. The effects of the modification of immunosuppression on the replication of BKV and graft outcome were analyzed.

Results

Of a total of 35 patient evaluated for BKV infection, 20 tested positive in at least one BK virus test. Decoy cells in urine were detected in 13 of the 20 patients. Of these patients, 7 developed BKV nephropathy. Four out of seven of the BKV nephropathy patients were diagnosed with biopsy, and the other three were diagnosed based on a high titer of BKV replication detected in plasma samples. Despite the reduction in immunosuppression and use of leflunomide in the seven BKV nephropathy patients, two patients suffered deterioration of renal function and one patient lost the graft with progressive renal dysfunction.

Conclusions

BK virus nephropathy was not an uncommon disease and was a major cause of graft dysfunction or loss. Appropriate modification of immunosuppressive therapy, early in the course of BK nephropathy or before the occurrence of massive replication of BKV, is essential for the protection of renal allografts.

Figures and Tables

Fig. 1
BK virus infection management algorithm based on our current practice.
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Fig. 2
Flow diagram depicting clinical outcomes of 20 patients of BK virus infection. Abbreviations: U, urine BK virus DNA PCR; S, serum BK virus DNA PCR; BKVN, BK virus nephropathy.
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Fig. 3
Clinical course of patient 1 (A) and patient 2 (B) who accompanied by concomitant acute rejection. Abbreviations: AR, acute rejection; BKVN, BK virus nephropathy; IVIG, intravenous immunoglobulin; Tac, tacrolimus; MMF, mycophenolate mofetil; ATG, antithymocyte globulin.
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Table 1
Clinical profiles of 7 patients with BK virus nephropathy
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Abbreviations: HTN, hypertensive nephropathy; PCKD, polycystic kidney disease; HSP, Henoch-Schonlein purpura; Tac, tacrolimus; MMF, mycophenolate mofetil; PDS, prednisolone; Bx, basiliximab; CNI, calcineurin inhibitor; BKVN, BK virus nephropathy; IgAN, IgA nephropathy.

Table 2
Diagnosis, treatment and clinical outcome of 7 patients with BK virus nephropathy
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Abbreviations: SV 40, simian virus 40; ND, not done; BKVN, BK virus nephropathy; CNI, calcineurin inhibitor; Tac, tacrolimus; CsA, cyclosporine A; MMF, mycophenolate mofetil; AR, acute rejection; Cr, creatinine.

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