In the current study, the frequency of BKV was 46.7% in cases and 30% in controls. The frequency of JCV was 23.3% in both groups. Post-transplant time in case group was significantly shorter in JCV positive than in JCV negative patients. This may indicate that in these patients, JCV infection may predispose to earlier graft dysfunction. In control group with normal allograft function, JCV was found in older patients.
Frequency of JCV in our study (23.3%) was similar to that reported in other studies, ranging from 13.7 to 36.8%,6,11,14,15
and occurred at a higher frequency in comparison to López et al. study.16
Also Frequency of BKV (38.3%) was higher in comparison to 6.815
and lower in comparison to 56.3%6
but was similar to López et al. study 40.7%.16
This could be attributable to different study designs and follow-up sampling timings.
In accordance with Drachenberg et al.6
the present study showed that in kidney transplant recipients (control group), the frequency of JCV in older patients was more than in younger ones. Some studies showed that whenever JC virus has been identified in the kidney of a patient with interstitial nephritis, BK virus has also been identified and JC virus alone has not been shown to cause interstitial nephritis.18,19
But in the present study, JC and BK virus has been identified in one patient. Different methodology and small sample size may be the possible reasons. Muller et al.20
found urinary JC virus excretion in 32% of renal transplant recipients which was in accordance with present study (23.3%). However, no correlation with allograft nephropathy was recognized. The role of JC virus in polyomavirus-associated nephropathy remains unclear, although evidence for JC virus participation in virus nephropathy of renal transplant recipients was previously observed.19
Ramos et al.21
demonstrated that patients diagnosed with polyomavirus presented with variable deterioration of graft function manifested by an increased serum creatinine. That was inconsistent with our results which showed there was no association between serum creatinine with the detection of polyomavirus.
Cheng XS et al. detected BKV and JCV in the urine samples of 35% and 16% of their patients, respectively, which was nearly the same as 46.7% and 23.3% in our case group and 30% and 23.3% in our control group, respectively.22
They also followed co-infection of both viruses and concluded that infection with either polyomavirus decreases the chance of infection with the other. In our study, also co-infection of both viruses was found only in one patient in the case group.
Saundh BK and coworkers, in the retrospective analysis of urine and plasma samples from 30 renal transplant patients found that eight patients (26.7%) were positive for BK viruria and five patients (16.7%) were positive for JC viruria. Rise in BKV and JCV antibody titers had association with high levels of viruria.
Although the number was similar to some cited studies,14,16,21,23
one limitation of the present study was the small number of patients enrolled. The other was lack of confirmation of the nephropathy by kidney biopsy because of unapproved protocol biopsy in our center. Some of our patients in case group were biopsied but it was not enough to make any conclusion that the renal failure is due to polyoma virus nephropathy.
Long-term studies with enough sample size are needed to define more information about the role of polyomavirus on graft function in kidney transplant recipients. Also, according to the other studies12,24,25
and our results, because of risk for this infections, screening during the first 24 months post-transplantation seems to be reasonable.