Collecting duct carcinoma arising in association with BK nephropathy post-transplantation in a pediatric patient. A case report with immunohistochemical and in situ hybridization study.

The development of malignancy in a renal transplant graft is an uncommon phenomenon. A renal neoplasm developing in the adult donor kidney of a pediatric transplant recipient has only rarely been reported. We report a case of collecting duct carcinoma arising in association with BK virus nephropathy in an adult living-related donor renal allograft to a pediatric recipient. Our case is the second report of neoplasia occurring in association with BK virus nephropathy post-transplantation, suggesting that BK virus may play a role in oncogenesis. It has been proposed that the T-Ag protein encoded by the polyomavirus family of viruses disrupts chromosomal integrity, creating oncogenes, and inactivating tumor suppressor genes. In our study, immunohistochemical staining with antibody directed against BK virus large T antigen showed nuclear staining within urothelium, tubular epithelium, tubular intraepithelial neoplasia, and invasive carcinoma. In situ hybridization did not identify BK virus DNA within neoplastic cells. T-Ag protein expression has been shown to be tumor-specific in bladder, gastric, and colorectal cancers. The finding of T-Ag protein expression in both intraepithelial and invasive neoplastic tissues in our case raises the possibility of BK virus as a causative agent in oncogenesis.

Management of cancer-associated thrombotic microangiopathy: what is the right approach?

A 49-year-old Caucasian woman presented with features suggestive of thrombotic microangiopathy (TMA). She did not respond to treatment with repeated plasma exchange and corticosteroids. A bone marrow biopsy revealed presence of metastatic carcinoma. A limited autopsy revealed presence of breast cancer with rib metastases. Though severe deficiency of von Willebrand factor-cleaving protease was initially proposed as a key pathogenetic factor for thrombotic thrombocytopenic purpura, subsequent studies involving patients with cancer-associated TMA did not find as severe a deficiency of von Willebrand factor-cleaving protease as is seen in idiopathic cases of thrombotic thrombocytopenic purpura. Here we address one approach of management of these patients with cancer-associated TMA.