Prognosis of BK Polyomavirus Nephropathy: 10-Year Analysis of 133 Renal Transplant Recipients at a Single Center
BK virus-associated nephropathy (BKVN) is a significant cause of chronic allograft dysfunction in renal transplant recipients. This study aimed to evaluate the prognosis of BKVN by retrospectively analyzing data from 133 renal transplant recipients treated at the First Affiliated Hospital of Sun Yat-Sen University between July 2007 and July 2017. The study compared BK viral loads, graft function, and pathologic indices between the initial diagnosis and the last follow-up.
Background and Significance
BK virus (BKV) infection is a common complication in renal transplant recipients, occurring in 10% to 60% of patients, with BKVN incidence as high as 10%. Approximately 10% to 50% of patients with BKVN develop progressive renal dysfunction, leading to eventual allograft loss. The management of BKVN involves reducing immunosuppression, which can complicate the clinical course by increasing the risk of acute rejection. This study provides a comprehensive analysis of the clinical features, treatments, and outcomes of BKVN in a large cohort of renal transplant recipients.
Patient Characteristics
The study included 133 renal transplant recipients with biopsy-proven BKVN. The mean age of the patients was 39.8 years, with a male-to-female ratio of 63.9% to 36.1%. Most recipients (84.2%) received deceased donor kidneys, and the majority (97.7%) were maintained on tacrolimus, mycophenolic acid, and glucocorticoids. The primary indication for biopsy was an elevation in serum creatinine (78.9%), and the mean follow-up period after BKVN diagnosis was 14.4 months.
Diagnosis and Pathologic Staging
BKVN was diagnosed based on renal biopsy and immunohistochemistry analysis, with SV40-T antigen staining confirming the presence of BK virus. According to the American Society of Transplantation (AST) criteria, 16.5% of patients were classified as stage A, 72.2% as stage B, and 11.3% as stage C. The median onset of biopsy-proven BKVN was 8.5, 14.4, and 27.0 months post-transplantation for stage A, B, and C patients, respectively. At the time of biopsy, BK viruria was present in 97.7% of patients, and BK viremia was present in 76.7%.
Graft Function and Outcomes
At the last follow-up, the mean estimated glomerular filtration rate (eGFR) was significantly lower than at the time of BKVN diagnosis (18.3 ± 9.2 vs. 32.8 ± 20.6 mL/min/1.73 m²). Five patients (3.8%) lost their graft function at the time of BKVN diagnosis, and an additional 13 patients (9.8%) lost their graft during the follow-up period. The 1-, 3-, and 5-year graft survival rates after BKVN diagnosis were 99.2%, 90.7%, and 85.7%, respectively. Higher pathologic stages of BKVN were associated with lower allograft survival rates.
Evolution of BK Viruria and Viremia
During the follow-up period, BK viruria became negative in 19.5% of patients, and BK viremia became negative in 90.2% of patients. The median time for the viral load to decrease by more than 90% was 2.5 months in urine and 2.8 months in plasma. The median time for plasma viral load to become negative was 4.0 months. Patients with persistent BK viruria and viremia had similar graft outcomes to those without persistent viral loads, suggesting that persistent viruria alone may not significantly impact graft function.
Rejection and Graft Outcomes
Eight patients (6.0%) developed acute rejection after reducing immunosuppression for BKVN management. At the last follow-up, the eGFR was significantly lower in patients with subsequent rejection than in those without (21.6 ± 9.8 vs. 33.5 ± 20.9 mL/min/1.73 m²). However, graft loss rates were similar between the two groups, indicating that while rejection negatively impacts graft function, it may not significantly increase the risk of graft loss in this cohort.
Pathologic Progression and Repeat Biopsies
Repeat biopsies were performed in 65 patients (48.9%) to evaluate the evolution of pathologic damage. SV40-T antigen staining remained positive in 40 patients and became negative in 20 patients. Patients with negative SV40-T antigen staining had significantly lower eGFR, urine viral loads, and plasma viral loads compared to those with persistent BK involvement. The degree of SV40-T antigen staining decreased over time, but interstitial fibrosis and tubular atrophy increased, highlighting the progressive nature of renal scarring in BKVN.
Discussion
This study underscores the importance of early diagnosis and management of BKVN in renal transplant recipients. The findings suggest that higher pathologic stages of BKVN at diagnosis correlate with worse graft outcomes, emphasizing the need for timely intervention. Reduction of immunosuppression was effective in clearing BK viremia but not viruria, indicating that persistent viruria may not significantly impact graft function. However, patients with persistent BK involvement in tissue had worse outcomes, highlighting the need for close monitoring and repeat biopsies to assess disease progression.
The study also highlights the challenges of managing secondary rejection after BKVN. While the incidence of rejection in this cohort was lower than previously reported, patients with subsequent rejection had significantly lower eGFR, underscoring the importance of balancing immunosuppression reduction with the risk of rejection. The progressive nature of renal scarring observed in repeat biopsies further emphasizes the need for strategies to inhibit renal sclerosis and delay graft function deterioration.
Conclusion
In conclusion, this 10-year analysis of 133 renal transplant recipients with BKVN provides valuable insights into the prognosis and management of this challenging condition. The study highlights the importance of early diagnosis, careful reduction of immunosuppression, and close monitoring of graft function and viral loads. Persistent histologic infection and secondary rejection are key factors associated with poor outcomes, underscoring the need for individualized treatment strategies to optimize graft survival in patients with BKVN.
doi.org/10.1097/CM9.0000000000000085
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