*Purpose: Cytomegalovirus (CMV) and BK polyoma virus are opportunistic infections after renal transplant (RTX) that have negative allograft outcomes. Immunosuppressive reduction is the mainstay of treatment for BK infection. Reduction of immunosuppression has been shown to have equivalent efficacy as antivirals in the treatment of CMV infection. As such, treatment of BK infection would be theorized to prevent future CMV infection for the duration of reduction in immunosuppression. However, there is no available literature describing the sequence of these events. Our objective was to evaluate the risk of CMV infection after BK infection.

*Methods: Observational single-center study of renal transplant (RTX) recipients transplanted between 1/1/2005-6/30/2014. Patients were excluded if the following events occurred in the first 3 months post-transplant; death, organ failure, lost to follow up, BK or CMV infection. Follow-up began 3 months after transplantation and BK was treated as a time-varying exposure with 1 year follow up.

*Results: 2295 RTX recipients met inclusion criteria; of these 423 developed BK during follow-up (BK+). In the BK+ group, 52 recipients developed CMV versus 215 in BK- group. Patients that did not develop BK and the BK+ population were similar in age, gender, BMI, prior transplant and receipt of living donor allograft. The proportion of the population that was CMV high-risk serostatus (D+/R-) was also similar between groups (BK+ 19.4% vs BK- 17.8%, p=0.44). There were significantly more African Americans in the BK+ group (BK+ 16% vs BK- 9%, p<0.01) and patients with primary renal disease due to polycystic kidney disease in the BK- group (BK+ 15.2% vs BK- 8.3%, p<0.01). BK occurred at a median of 109 days (Q1 66, Q3 215) post-transplant, after exclusion for any occurrence in the first 90 days. In those with subsequent CMV infection after BK, CMV occurred at a median of 80 days (Q1 -59, Q3 159) after BK diagnosis. BK+ was associated with lower risk of CMV infection, but this was not statistically significant (BK+ HR 0.84, 95% CI 0.61-1.19, p=0.34). When adjusted for age, gender, race, BMI, prior transplant, living donor and high-risk serostatus, the incidence of CMV infection remained reduced in the BK+ population, but not significantly (BK 0.83, 95% CI 0.58-1.17, p=0.29).

*Conclusions: The risk of incident CMV infection is lower in patients with a history of BK infection, but this did not reach statistical significance. While CMV has been shown to co-infect with other opportunistic infections, likely due to its immunomodulatory effects, this may not be true for BK infection, particularly given resultant reduction of iatrogenic immunosuppression used in treatment. Future studies are needed to better elucidate the interplay of these viral infections after renal transplant.

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