To explore the effect of BK virus viremia on the recipient and the function of transplant kidney after transplantation.

The clinical data of 229 recipients who received kidney transplantation in the First Affiliated Hospital of University of Chinese Academy of Sciences were analyzed retrospectively. According to the maximum serum BK virus load within 24 months after transplantation, the recipients were divided into virus-free group (serum BKV continued negative), low virus load group (serum BKV maximum load≤1×10⁴ copies/mL) and high virus load group (serum BKV maximum load>1×10⁴ copies/mL). The estimated glomerular filtration rate (eGFR) was used to evaluate the kidney function. The age and gender of the recipients, the source of the donor kidney, the time of cold/hot ischemia of the donor kidney, the immunosuppressive program, the blood trough concentration of tacrolimus at 3 months after transplantation, the incidence of rejection and graft dysfunction, and the eGFR within 24 months after transplantation was observed. Single factor analysis of variance was used to compare the age of recipients, the time of cold/hot ischemia of donor kidney, the blood trough concentration of tacrolimus at 3 months after transplantation and eGFR in 24 months after transplantation in the 3 groups and that between groups with LSD method. Group t test was used to compare the first detection time of BK virus infection between the low virus load group and the high virus load group. Chi square test was used to compare the source of donor kidney, immunosuppressive regimen, and the incidence of graft failure and rejection. P<0.05 was statistically significant.

BK virus viremia was detected in 64 recipients among 229 recipients (28%), of which 19% (43/229) was low virus load and 9% (21/229) was high virus load. As of July 2018, the average follow-up time of 229 recipients was (44±8) months. The first detection time of BK virus infection was (10±8) months after transplantation in low virus load group and (8±6) months in high virus load group, which had statistical significance (t=2.10, P<0.05). The rejection rate of virus-free group [24.8% (41/165)] was lower than that of low virus load group [60.5% (26/43)] and high virus load group [61.9% (13/21)] (χ²=19.82 and 12.42, P all<0.017). The incidence of cellular rejection in virus-free group [13.9% (23/165)] was lower than that in low virus load group [39.5% (17/43)] and high virus load group [42.9% (9/21)] (χ²=14.38 and 10.94, P<0.017). 12 recipients in the virus-free group, 2 recipients in the low virus load group, 4 recipients in the high virus load group (3 with BK virus associated nephropathy, 1 with unclear etiology) had renal allograft dysfunction, which had no statistical significance (χ²=4.727, P>0.05). The blood trough concentration of tacrolimus at 3 months after transplantation in the high viral load group was higher than that in the virus-free group and the low virus load group (P all<0.05). At the 3th, 6th, 12th and 24th month after operation, eGFR of the recipients in the high virrus load group were all lower than that in the virus-free group and the low virus load group (P all<0.05).

High BK virus viremia after kidney transplantation can significantly affect the prognosis of recipients; low BK virus viremia had no significant adverse effect on the function of transplant kidney, and there was no need to adjust the dosage of tacrolimus for recipients with low BK virus viremia.