The two human polyoma species, JC and BK, were isolated from patients with the same initials in 1971. Polyoma virus can cause interstitial nephritis and lead to graft failure in renal transplant recipients. For JC, most persons become seropositive by the age of 10; for BK, the majority of persons are seropositive by 5. By adulthood, 70-90% of individuals have antibodies to both JCV and BKV. The viruses contain a seroprevalence rate of about 50% for JC and about 90% for BK virus in the age group of 9–11 years.^3,4 BK virus -related nephropathy was detected in about 8% of renal allograft recipients with loss of renal allograft ranging from 10% to 80% of cases.⁵ Only a few cases of nephritis have been credited to JCV, and now limited information is available with respect to JCV replication in kidney transplant patients and its impact on graft function.⁶ Studies showed that 1 to 7% of renal transplant recipients developed polyomavirus nephropathy,^7,8 and the incidence appears to be growing.⁹ More than 45% of renal transplant recipients who develop BK nephropathy lose their grafts due to infection.¹⁰ Also, as reported in a clinical study, graft dysfunction attributed to viral infection occurred in 38% of patients with BKV shedding and no patients with JCV shedding.⁶ A study by Costa et al. showed that BKV was positive in 32 of 109 patients (29.6%) and JCV in 20 of 109 patients (18.3%) with renal allograft.¹¹

The number of patients with ESRD on the waiting list for a renal transplant has continued to increase at a steady rate. Any attempts to prolong kidney survival may improve this situation. Polyomavirus have emerged as an important cause of renal allograft failure. There are no agreement guidelines for the detection, prevention, and treatment of polyomavirus infection in transplant recipients. But, screening for polyomavirus is recommended at centers that have experienced high rates of polyomavirus infection.¹² The aim of this study was to compare the frequency of BKV and JCV infections in renal transplant recipients with and without graft dysfunction.

In all patients, data obtained included recipient demographic characteristics, immunosuppressive regimen (the immunosuppressive regimen in two groups after transplantation included induction with methylprednisolone and maintenance triple therapy with prednisolone, cyclosporine and mycophenolate mofetil), duration of dialysis, time after transplant and laboratory data including serum creatinine level. For each patient, first morning urinary sample was obtained and evaluated for BK and JC virus detection in our laboratory.

BKV and JCV were extracted from urine samples with QIAamp DNA Mini Kit and quantified by real-time polymerase chain reaction.¹³ Virus copies more than 100 copies/ml considered to be positive. Figure 1 shows the result of JC and BK virus detection by polymerase chain reaction by visualization of bands of the appropriate size on agarose gels after electrophoresis.

In the study population, 14/60 (23.3%) patients (case group, seven; control group, seven) were positive for JC virus and 23/60 (38.3%) patients (case group, fourteen; control group, nine) were positive for BK virus. No significant difference was observed between case and control groups of either virus. Results are summarized in Table 2. JCV was detected alone in 13 patients (case group, six; control group, seven); BKV was detected alone in 22 patients (case group, 13; control group, 9); both JCV and BKV just were detectable in one patient in case group.

As shown in Table 3, the Mann-Whitney U test revealed that the median post-transplant time in patients with acute deterioration of their kidney function was significantly shorter in JCV positive than in JCV negative patients [4 (3.7-5.5) vs. 10 (6-19) months], (P = 0.003). Also, within controls the median age were 60 (45-61) years in patients with JCV positive and 40 (29-57) years in patients with JCV negative; this difference was also statistically significant (P = 0.04).

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, 18.3¹¹, 13.1%¹⁷ 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.