Polyoma virus infection and urothelial carcinoma of the bladder following renal transplantation

Renal transplant recipients are at increased risk of bladder carcinoma. The aetiology is unknown but a polyoma virus (PV), BK virus (BKV), may play a role; urinary reactivation of this virus is common post-renal transplantation and PV large T-antigen (T-Ag) has transforming activity. In this study, we investigate the potential role of BKV in post-transplant urothelial carcinoma by immunostaining tumour tissue for PV T-Ag. There was no positivity for PV T-Ag in urothelial carcinomas from 20 non-transplant patients. Since 1990, 10 transplant recipients in our unit have developed urothelial carcinoma, and tumour tissue was available in eight recipients. Two patients were transplanted since the first case of PV nephropathy (PVN) was diagnosed in our unit in 2000 and both showed PV reactivation post-transplantation. In one of these patients, there was strong nuclear staining for PV T-Ag in tumour cells, with no staining of non-neoplastic urothelium. We conclude that PV infection is not associated with urothelial carcinoma in non-transplant patients, and is uncommon in transplant-associated tumours. Its presence in all tumour cells in one patient transplanted in the PVN era might suggest a possible role in tumorigenesis in that case

Urological malignancy after renal transplantation.

Immunosuppression in solid-organ recipients is associated with a greater risk of de novo malignancy after transplantation; herein we report the UK transplant registry (UKTR) database of urological cancer after renal transplantation in the UK transplant population. From September 1999 to January 2006 there were 10,847 kidney recipients with at least one period of follow-up reported after a kidney transplant (mean age at transplantation 42.4 years, sd 15.5; 6685 male, 61.6%, and 4162 female, 38.3%). The recipients represent a homogenous group who received different immunosuppression regimens. Skin cancer was excluded from the study. Unfortunately, the UKTR does not collect information about the presence or absence of cancer, either at registration onto the transplant waiting list or at transplantation. In all, 214 (1.9%) patients were reported to have a subsequent urological malignancy diagnosed among the 10,847 recipients. The UKTR was used to identify patients who developed urological malignancies after renal transplantation, which is a challenging event after solid-organ transplantation. Regular surveillance to diagnose early occurrence and adjustment of immunosuppression might be beneficial. In the presence of metastatic disease, chemotherapy treatment with adjustment or cessation of immunosuppressive therapy is required

Polyoma virus infection and urothelial carcinoma of the bladder following renal transplantation.

Renal transplant recipients are at increased risk of bladder carcinoma. The aetiology is unknown but a polyoma virus (PV), BK virus (BKV), may play a role; urinary reactivation of this virus is common post-renal transplantation and PV large T-antigen (T-Ag) has transforming activity. In this study, we investigate the potential role of BKV in post-transplant urothelial carcinoma by immunostaining tumour tissue for PV T-Ag. There was no positivity for PV T-Ag in urothelial carcinomas from 20 non-transplant patients. Since 1990, 10 transplant recipients in our unit have developed urothelial carcinoma, and tumour tissue was available in eight recipients. Two patients were transplanted since the first case of PV nephropathy (PVN) was diagnosed in our unit in 2000 and both showed PV reactivation post-transplantation. In one of these patients, there was strong nuclear staining for PV T-Ag in tumour cells, with no staining of non-neoplastic urothelium. We conclude that PV infection is not associated with urothelial carcinoma in non-transplant patients, and is uncommon in transplant-associated tumours. Its presence in all tumour cells in one patient transplanted in the PVN era might suggest a possible role in tumorigenesis in that case