BK VIRUS INFECTION

R.P. Singh¹, T.B. Dunn², R. Kandaswamy³, R. Fairchild¹, K.J. Gillingham⁴, W.D. Payne¹, T.L. Pruett³, D.E. Sutherland⁵, A.J. Matas⁴, E.B. Finger^1
1Department Of Surgery, University of Minnesota, Minneapolis/MN/UNITED STATES OF AMERICA, ²Surgery, Univ of Minnesota, Minneapolis/UNITED STATES OF AMERICA, ³Surgery, University of Minnesota, Minneapolis/MN/UNITED STATES OF AMERICA, ⁴Department Of Surgery, University of Minnesota, Minneapolis/UNITED STATES OF AMERICA, ⁵Surgery, University of Minnesota, Minneapolis/UNITED STATES OF AMERICA

Body: Purpose: Identifying the risk factors (RF) for developing polyoma virus infection (PVI) after kidney transplantation. Methods: Retrospective analysis of consecutive adult kidney transplant recipients (KTRs) in a single center using binary logistic regression analysis. PVI was diagnosed as BK viremia detected by polymerase chain reaction, or by histopathological evidence of BK viral infection confirmed by SV 40 staining. Results: Total of 1498 KTRs during the period from 01/2000 to 02/2009 were studied. Minimum period of follow-up was 1 year (range 1-10 yrs). PVI was seen in 53 (3.5%) KTRs and seen after a mean period of 15 months post-transplant. KTRs with PVI had significantly poor actuarial graft survival (67% for PVI vs. 86% for No PVI, p=0.008, log rank test) but no difference was seen in patient survival (93% for PVI vs. 90% for No PVI cohort, p=NS, log rank test) after 5 years post-transplant. Univariate analysis showed that PVI was significantly associated with multiple acute rejection (AR) episodes (16% vs. 3%, p=0.0001), treatment of ARs (21% vs. 10%, p=0.03) with antibodies (thymoglobulin or OKT3) and male KTR (4% vs. 1.6%, p=0.01). There was no association of PVI with single acute rejection (27% vs. 22%), treatment of rejections with steroids alone, treatment of humoral rejections, use of tacrolimus/mycophenolate mofetil combination, use of thymoglobulin induction, recipient age or expanded criteria donor kidneys. The use of rapamycin showed a trend of negative association (5% vs. 12%, p=0.1) with development of PVI. Both CMV (34% vs. 25%) and BK (43% vs. 25%, both p<0.01) were significantly associated with AR episode, but the development of CMV infection did not predispose to development of PVI. Multivariate analysis showed multiple episodes of AR (p=0.009, Odds Ratio 4.1, CI 1.4-11.9) and male KTRs (p=0.008, OR 2.7, CI 1.2-5.7) to be the most significant RFs for developing PVI, whereas the use of antibodies for treating ARs lost significance. Subgroup analysis showed that PVI was significantly associated with cellular (43% vs. 24%, p=0.004), but not with humoral rejection (11% vs. 8%). PVI was associated with early (within 1^st year) rejections (34% vs. 20%, both p<0.01). PVI associated with AR was seen to occur slightly earlier in the post-transplant period compared to PVI without AR episode (17 vs. 27 months). PVI was seen to occur after a mean of 6.6 months (SD 10.8) after the treatment of AR episodes. Conclusion: Polyoma viral infection is associated with poorer graft survival. It has a significant association with multiple episodes of acute rejection. The associations were stronger with cellular and early post-transplant rejection episodes. It is unclear whether multiple acute rejections are a risk factor on their own accord, or whether the treatment of multiple ARs with various immunosuppressive agents generates a milieu conducive for developing PVI. Male recipient gender is a RF for developing PVI which maybe explained due to hormonal factors.

Disclosure: All authors have declared no conflicts of interest.