Introduction: BK virus-associated nephropathy (BKVN) represents a significant cause of renal graft dysfunction and graft loss, while the optimal therapeutic approach for patients with BKVN has not been established. This study presents the therapeutic management for kidney transplant recipients with BKVN and transplant outcomes, along with a comparative analysis of renal transplant outcomes compared with a control group.
Materials and Methods: A retrospective study was conducted on patients transplanted from living or deceased donors, from January 2005 to June 2023, including all patients who developed BKVN. BKVN was defined as the presence of PCR BKV > 10.000 copies/mL for more than one month with concomitant deterioration of renal function and characteristic BKV infected cells on cytologic examination of the urine (decoy cells), or the presence of histologic features of polyomavirus infection on renal allograft biopsy. Matching with the control group was performed 1:1 based on age, gender, and transplantation characteristics.
Results: From a total of 1583 recipients, 194 recipients were included, of whom 97 developed BKVN at a median time of 3 months post-transplantation. A reduction of mycophenolate acid (mycophenolate mofetil/mycophenolate sodium) dosage occurred in 88% of patients, discontinuation in 57.7%, and calcineurin inhibitor (tacrolimus/cyclosporin) reduction in 82.5%. Leflunomide was administered in 48.5% of cases, while 14% of patients received intravenous immunoglobulin. Five percent of patients with BKVN developed de novo donor-specific antibodies (DSAs), and 5% experienced biopsy-proven acute rejection episodes (BPAR) within 6 months of BKVN onset. Patients with BKVN had worse renal graft function outcomes compared to the control group, eGFR (MDRD formula): 51 vs. 57.5 ml/min/1.73m² at 3 years (p=0.053), 49 vs.57ml/min/1,73 m² at 4 years, (p=0.043) and 51 vs. 56 ml/min/1.73m² at 5 years (p=0.076). Worse outcomes were observed in patients with PCR BK > 100.000 copies/mL, histologically proven BKVN or concomitant acute rejection episode. The risk of graft loss was significantly higher in BKVN patients (8% vs. 0%, p=0.007).
Conclusion: BKVN can lead to irreversible renal graft damage, while reduction of immunosuppression as the primary intervention entails the risk of de novo DSAs development and BPAR among renal transplant recipients. Establishing appropriate protocols for effective management is essential.