BK polyoma virus replication in de novo renal transplant recipients: Results of a prospective study
Abstract number: p759
Koukoulaki M., Grispou E., Saroglou G., Pistolas D., Balaska K., Apostolou T., Anagnostopoulou M., Hadjiconstantinou V., Paniara O., Drakopoulos S., Legakis N.
BK polyoma virus has been associated with the development of renal allograft interstitial nephritis, which may lead to chronic allograft dysfunction. This study evaluated prospectively the replication of BK polyoma virus in renal transplant recipients.
Thirty-two de novo renal transplant recipients of median age 48.5 years old were studied for mean follow up period of 36 weeks. Plasma and urine samples were collected at three monthly intervals after renal transplantation and examined for BKV with qualitative and quantitative real time polymerase chain reaction (PCR). All recipients received anti interleukin-2 receptor monoclonal antibody and triple immunosuppression regimen with calcineurin inhibitor (cyclosporine, n = 19, or tacrolimus, n = 13), mycophenolate mofetil and oral corticosteroids. A total of 340 samples were examined (170 and 170 urine plasma).
BKV was detected in 53 (31.2%) urine and 30 (17.6%) plasma samples in 22 (22/32, 68.8%) and 19 (19/32, 59.4%) patients respectively. Positive samples for BKV simultaneously in urine and plasma were observed in 22 cases (22/170, 12.9%). Quantification of positive urine samples identified 18 with viral load > 10,000 copies/ml which were collected from 10 individuals. Quantification of positive plasma samples showed that two patients had viral load above 10,000 copies/ml that also had high viral load in urine. Relative risk of BK viraemia was 5-fold in recipients who had developed BK viruria (R.R. 5, 95% confidence interval 3.39.7). Median time of onset of viruria was 62 days after transplantation and of viraemia 72 days following transplantation. A peak of viraemia and viruria with high viral load in urine was noted 3 months after renal transplantation. Statistical analysis of the immune suppressive regimens revealed that incidence of BK viruria was significantly higher in patients who received tacrolimus compared to cyclosporine (p = 0.005). Statistical analysis of serum creatinine between positive and negative cases in plasma and urine of BKV revealed no significant difference or impairment of renal allograft function.
BK viruria precedes BK viremia. High viral load in plasma was accompanied in all cases with high viral load in urine, which suggests that viruria is a risk factor of the development of viraemia. Significant relation was observed between positive urine samples for BKV and tacrolimus immunesuppressive treatment.
|Session name:||XXIst ISTH Congress|
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