Increased Rates of BK Virus-Associated Hemorrhagic Cystitis and BK Viremia in Haploidentical Stem Cell Transplantation

Abstract

Introduction In haploidentical transplantation, increased infectious risk compared to matched related donor (MRD) and matched unrelated donor (MUD) transplants is a complication that contributes to patient morbidity and mortality. This study investigated the 1-year post-transplant rates of BK virus-associated hemorrhagic cystitis and BK viremia in the haploidentical population compared to the non-haploidentical population. Objectives The objectives of this study were to compare the rates of BK virus-associated hemorrhagic cystitis and BK viremia in haploidentical patients compared to MRD and MUD patients within 1 year after transplant. In addition, we investigated whether patients with BK virus-associated hemorrhagic cystitis were at higher risk for also developing BK viremia in the haploidentical population. Methods This was a retrospective study that analyzed the outcomes of patients who underwent allogeneic stem cell transplants from haploidentical donors, MRD, or MUD. BK virus infection was assessed through urine samples and via a quantitative serum detection test. Statistical analysis was performed using the Fisher Exact Probability Test with p-values Results Out of 174 transplant patients, 44 (25%) transplants were from haploidentical donors and 130 (75%) from non-haploidentical donors (MRD and MUD). BK viruria was detected in a significantly higher amount of haploidentical patients, with 15 (34%) haplo and 13 (10%) non-haplo patients affected (p = 0.004). All cases of BK viruria were associated with hemorrhagic cystitis. The rate of BK viremia was also significantly higher in the haploidentical population, affecting 7 (16%) haplo patients vs. 1 (0.1%) non-haplo patient (p Conclusion Our results indicated that amongst the haploidentical population, there were significantly higher rates of BK virus-associated hemorrhagic cystitis and BK viremia compared to the non-haploidentical population. In addition, out of all allogeneic transplant patients who were found to have BK viruria, a frequently reported infection in the transplant population, haploidentical patients were at greater risk of developing BK viremia as well. These findings were also in the context of similar rates of GVHD between haplo and non-haplo patients, indicating that the higher rates of infections were not due to increased GVHD immunosuppression. Further investigation is warranted to confirm these findings and propose prophylactic approaches to BK virus infections in the haploidentical population.