INFLUENCE OF BK VIRUS PLASMA VIRAL LOAD IN KIDNEY TRANSPLANT OUTCOMES

Abstract BACKGROUND AND AIMS BK virus infection (BKi) is an important cause of kidney transplant (KT) loss. Besides to reducing immunosuppression, the rest of the therapies have not shown a clear benefit. Our purpose is to analyze the risk factors for BKi and the influence of BK plasma viral load on KT outcomes. METHOD Prospective cohort study of KT with BKi, defined by the presence of BK viremia in ≥3 consecutive determinations, from 01 January 2010 to 31 December 2020. BK viremia was determined every 10 days during the first 3 months, at 6th month, 12th month and in case of impaired renal function. In patients with positive viremia, immunosuppressive therapy was changed (reduction/discontinuation of mycophenolate and/or switching to everolimus). Patients with high-level viremia (≥10 000 copies/mL) and low-level viremia (<10 000 copies/mL) were compared. To identify risk factors for BKi, for each KT with BKi, we selected two matched controls and performed a logistic regression analysis. Graft survival was analyzed according to BK viremia (high-level, low-level and negative) using Kaplan–Meier and Cox regression analysis was performed to determine risk factors for graft survival. RESULTS 849 KT were performed, of which 67 (7.9%) presented BKi. Six KT were excluded due to incomplete data. Finally, 61 KT BKi (n = 27, high-level viremia; n = 34 low-level viremia) and 122 controls were analyzed. The median post-KT time to BKi was 2 months. In the multivariable analysis, male recipient, older age and re-KT were risk factors for BKi. Proven BK-associated nephropathy was diagnosed in five KT recipients and nine patients had persistent BK viremia, all of them from the high plasma viral loads group. Only one patient lost the graft due to BK-associated nephropathy. Patients with low-level viremia had worse renal function one month after KT than controls but without differences at the first year. Patients with high-level viremia had worse renal function one year after KT and worse graft survival than recipients with low-level viremia and controls (P = 0.037). In the multivariable analysis, when we analyzed exclusively patients with BKi, high-level viremia was a risk factor for kidney graft survival (HR: 16.31; P = 0.034). CONCLUSION BKi is not an uncommon complication after KT. Only high BK viral load was associated with BK-associated nephropathy, persistent viremia, and poorer graft survival. BK viremia <10 000 copies/mL did not affect KT outcomes. Therefore, monitoring BK plasma viral loads and changes in immunosuppression to reduce viremia are effective strategies to minimize the impact of BK virus on graft survival.