Elsevier

Transplantation Proceedings

Volume 35, Issue 6, September 2003, Pages 2196-2198
Transplantation Proceedings

Renal transplantation: complications: infections
Polyomavirus BK infection

https://doi.org/10.1016/S0041-1345(03)00818-2Get rights and content

Abstract

Because it is an important factor affecting renal transplant function, BK infections are significant problem in posttransplant. BK nephropathy develops in 5% of renal allograft recipients, in most cases within the first year after the procedure. The gold standard for BK nephropathy diagnosis is still immunohistochemical staining for large T antigen in graft biopsy specimens. The aim of the present study was to evaluate the incidence of and factors influencing BK nephropathy in our renal allograft population. Among 89 renal or pancreas/kidney allograft recipients, BKV DNA was detected in 1 or more serum samples in 17 patients but BK nephropathy was diagnosed in only 1 case. Plasmacytic tubulitis was an exclusive feature in PCR-positive patients with 2 (20%) cases but no such findings in the PCR-negative group. In 40% of patients in the PCR-positive group at least 1 rejection episode was diagnosed versus 22% in the PCR-negative group. There were no significant differences in both groups according to total ischemia time, immunosuppressive treatments, or mean serum creatinine at 1 year after transplantation.

Section snippets

Patients and methods

From the 89 renal or pancreas/kidney allograft recipients in our center in 2001 and 2002, we collected blood samples at the end of 1, 3, 6, and 12 months. All specimens were tested with the PCR technique for BKV DNA. In cases of increased creatinine levels, a renal allograft biopsy was performed. In addition to routine histopathological examination, biopsy specimens were stained for the T antigen SV 40, which shows a 98% protein homology with BKV.

Results

BKV DNA was detected in 1 or more serum samples of 17 patients at a mean of 27 weeks after transplantation (range, 4–25 weeks). A biopsy was performed at least once in 45 patients in the study group, 10 of whom were BKV DNA–positive. BK nephropathy was diagnosed in only 1 case.

Acute interstitial rejection (IA or IB according to Banff 1997) was observed in 4 (40%) of 10 PCR-positive patients versus 4 (11%) of 35 in the PCR-negative group. Acute vascular rejection (IIA according to Banff 1997)

Discussion

The vast majority of BK nephropathy was observed in renal allografts but not in native kidneys, implying that there is a specific risk factor for graft recipients. Among others, ischemia and immunosuppressive drugs have been suggested. In our study, treatment with MMF and ischemia time were not risk factors for BKV replication. We did observe an increased incidence of CMV infection in patients with signs of BKV replication, but this may be attributed to the general susceptibility of those

Conclusions

The results suggest that graft function in patients with signs of BKV replication (but without BK nephropathy) was the same as in patients with no viral replication. Acute rejection may contribute to viral replication. There were positive correlations between serum BKV replication and histopathological findings of plasma cell infiltrates and plasmacytic tubulitis, features that may be helpful to select patients likely to experience BK nephropathy. In our opinion, these patients require close

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