Introduction: Polyomavirus-associated nephropathy (PVAN) occurs in 5% of renal transplant recipients (RTR) and is caused by Polyomavirus BK (BKPyV) and JC (JCPyV), at a very low rate. This disease causes a progressive impairment of renal function and ultimate graft loss. Monitoring of viral load with pre-emptive reduction of immunosuppression is the only proved preventive strategy to reduce the risk of PVAN. The aim of this study was to describe the evolution of BKPyV and JCPyV viral load in de novo pediatric RTR.

Method: A prospective observational study was carried out in a pediatric RTR. Paired samples of serum and urine were collected at baseline (on the day of transplantation), then monthly for at least 9 months post transplantation (PostTx). Viral load of BKPyV and JCPyV was determined by a Multiplex Real Time PCR assay (transferred by Fedele CG,2012).

Results: Fourteen patients were enrolled, the median age of the group was 13 years old (8-19) and 11 were male. The monitoring period was from 9 to 20 months (media 16). None of the patients developed PVAN during the study, but 11 (78%) of them tested positive, which were divided into three groups:

1. BKPyV positive (n=7) - they showed a pattern of viruria with a maximum between the 2^nd and 7^th month PostTx (median 8.5.10⁸copies/ml), after this peak viral load diminished significantly over the time getting undetectable in 4 cases. Two patients had higher values at the maximum in coincidence with impairment of renal function. Viremia was detectable in all cases, but with intermittences and it has not shown a well-defined profile, the highest values were around 10⁴copies/ml.
2. JCPyV positive (n=2) - both cases had JCPyV viruria without viremia with similar patterns: viral load was detectable from 2^nd month PostTx and continued along the time with tendency to increase.
3. BKPyV and JCPyV dual positive (n=2) - BKPyV viruria and viremia were detected at low rates at the beginning, then appeared JCPyV viruria simultaneously but with higher viral load, and from 10^th month PostTx to the end (17^th  month) only JCPyV viruria was detectable with the same upward trend as group two.

Conclusion: We detected active infection of BKPyV in 64% (9/14) of the cases, although there was no occurrence of any case of PVAN. However, in cases with impair renal function it were observed a significant increase of viruria. There are different proposed algorithms for monitoring BKPyV viral load to identify patients at risk of PVAN. We found a characteristic pattern of BKPyV viral shedding in urine. Based on this finding we would recommend to strengthen controls between 2^nd to 7^th month PostTx to be more sensitive to detect patients with viruria higher than 10⁷copies/ml, thus at more risk to develop viremia and consequently PVAN. Finaly, when PVAN is suspected and BKPyV is undetectable, JCPyV diagnose should be made, since it can cause PVAN as well although with low frequency, and we demonstrated its presence in 29% of the cases.