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Effect of Transient BK Viremia after T-Cell Depleting Antibody Therapy in Kidney Transplant Recipients, The

J. Sageshima, G. Ciancio, L. Chen, A. Mattiazzi, G. Guerra, W. Kupin, D. Roth, P. Ruiz, G. Burke III

Dept of Surgery, MTI, Miami
Dept of Medicine, Univ. of Miami Miller School of Medicine, Miami, FL

Meeting: 2013 American Transplant Congress

Abstract number: C1361

Polyoma BK virus-associated nephropathy (BKVN) is a significant cause of premature graft loss in kidney transplant recipients. Transient BK viremia is observed after an induction therapy; however, the natural course and the clinical significance of this phenomenon are unclear.

In this single-center retrospective study, we analyzed 527 patients who received kidney or kidney/pancreas transplantation and were screened for BK virus plasma PCR from Sep. 2008 to Dec. 2011. The patients were induced with T-cell depleting antibody +/- anti-IL2 receptor antibody, and maintained with tacrolimus-based immunosuppression. BK viremia and BKVN were treated initially by reduction of immunosuppressive medication, and in some cases, with leflunomide, ciprofloxacin, or intravenous immunoglobulin.

During the initial 3 mo after transplantation, 131 (24.9%) patients had at least one positive BK viremia. Of these patients, 69.5% continued to shed the virus beyond 3 mo post-TX. The viremic patients during the 3-mo period had a higher incidence of BKVN (6/131, 4.6%) than non-viremic patients (4/396, 1.0%, OR 4.704, p=0.0182). Both the patient survival (92.5% vs. 97.7%) and death-censored graft survival (89.1% vs. 97.4%) were inferior in the viremic patients (p=0.0259 and p=0.0009, respectively) as compared with non-viremic patients.

To further clarify the significance of “transient” viremia after the induction therapy, these 131 patients were divided into 2 subgroups: patients whose BK viremia disappeared after 1 mo until 3 mo (n=40, transient viremia) and patients who had viremia after 1 mo post-Tx (n=91, persistent viremia). None of the transient-viremia patients developed BKVN, whereas 6 persistent-viremia patients developed BKVN. There were no significant differences in patient and graft survival (92.5% vs. 92.6% at 3 years, p=0.9777 and 88.9% vs. 89.4%, p=0.8926) between groups, and they were worse than BK virus-negative patients.

In conclusion, BK viremia is relatively common after T-cell depleting antibody therapies with tacrolimus maintenance. BK viremia during 3 mo post-Tx is a significant risk factor for subsequent BKVN. Although transient BK viremia during 1 mo post-Tx was not associated with BKVN, poor patient and graft survival in this patient group may suggest a negative impact of BK viremia from other mechanisms.

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To cite this abstract in AMA style:

Sageshima J, Ciancio G, Chen L, Mattiazzi A, Guerra G, Kupin W, Roth D, Ruiz P, III GBurke. Effect of Transient BK Viremia after T-Cell Depleting Antibody Therapy in Kidney Transplant Recipients, The [abstract]. Am J Transplant. 2013; 13 (suppl 5). https://atcmeetingabstracts.com/abstract/effect-of-transient-bk-viremia-after-t-cell-depleting-antibody-therapy-in-kidney-transplant-recipients-the/. Accessed May 17, 2025.

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