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Association Between Donor/Recipient BK Viral Serostatus and Risk of BK Viraemia Post-Transplantation

Introduction The development of BK viraemia, and subsequently, BK nephropathy is a potentially devastating event associated with kidney transplant loss. In contrast to other clinically important viruses (e.g., CMV), donor and recipient BK serostatus is not routinely established pre-transplantation. It is therefore unclear whether active infection post-transplantation is donor-derived, due either to primary infection in a previously BK-naïve recipient or re-infection with a viral genotype not previously encountered, or recipient-derived, due to re-activation of latent virus as a consequence of immunosuppression. We investigated the BK serostatus of UK organ donors and examined the association of donor/recipient serostatus mismatch with development of BK viraemia post-transplantation. Methods Serum samples from 95 kidney donors, matched to 101 organs transplanted in our unit, were obtained from the national Quality in Organ Donation (QuOD) biobank; 10 recipients of these organs had developed BK viraemia (threshold >100 viral copies/ml). Donor serum was tested for BK IgG via ELISA, and for the presence of viral DNA. Recipient clinical data, including development of BK viraemia, time to/duration of viraemia, and peak viral load, were collected. Pre-transplant serum samples from 26 matched recipients, 5 with documented BK viraemia, were similarly analyzed and linked to donor serostatus. Results Of 95 donors evaluated, only 46 (48.4%) were seropositive for BK, none with detectable viraemia. 10/47 (21.3%) patients who received kidneys from BK seropositive donors developed BK viraemia, versus 6/54 (11.1%) patients who received kidneys from seronegative donors. The mean peak viral load was 100-fold higher in recipients of a kidney from a seropositive versus a seronegative donor (428331 vs 3293 copies/ml). Similar rates of BK seropositivity (14/26;53.8%) were seen in recipients pre-transplant. 4 (33.3%) seronegative recipients developed viraemia compared to 1 (7.1%) of seropositive recipients; 4/5 (80%) were seronegative pre-transplant, all 5 received a kidney from a seropositive donor. Conclusion In our pilot study, BK viraemia rates were increased in seronegative recipients, and in patients who received kidneys from seropositive donors. Our data suggest that determining the donor/recipient serotype mismatch may be a useful tool for stratifying the risk of BK disease.