Nasopharyngeal T-cell monomorphic posttransplant lymphoproliferative disorders and combined IgA nephropathy and membranous glomerulonephritis in a patient with renal transplantation: a case report with literature review.

Recurrent and/or de novo glomerular diseases occurring in a renal allograft have been reported in the literature and are an important cause of graft dysfunction and eventual loss. The simultaneous occurrence of two glomerulonephritis, although reported in the literature, is a rare phenomenon. Posttransplant lymphoproliferative disorders (PTLD) are well known and one of the most serious and potentially fatal complications of chronic immunosuppression in the solid organ transplant recipient. Here, we are reporting the first case, to the best of our knowledge, of simultaneous occurrence of nasopharyngeal monomorphic monoclonal PTLD and two distinctive glomerular diseases (IgA nephropathy and membranous glomerulonephritis) in a 49-year-old patient who was 5 years post-renal transplantation. We have provided the clinical history of our patient who presented with nephrotic range proteinuria, microscopic hematuria, and a nasopharyngeal mass as well as a review of the literature.

B- and T-Lymphocyte distribution in benign and malignant lymphoepithelial lesions of the parotid gland: Correlation with Epstein-Barr virus expression and a proposed mechanism of malignant transformation.

Epstein-Barr virus expression in malignant lymphoepithelial lesions (LEL) of the parotid gland has been well established. The virus is occasionally expressed in benign LEL, especially in immunocompromised hosts. The pathogenesis of the disease as it relates to virus expression and lymphocyte subsets has not been clearly defined. In this study, we attempted to identify B- and T-lymphocyte distribution in the lesions as it relates to EBV expression in LELs of the parotid gland. Formalin-fixed paraffin-embedded sections of 18 cases of LEL of the parotid gland were immunohistochemically tested for the distribution of B- and T-lymphocytes in the lesions, using the antibodies L-26 (CD 20) for B-lymphocytes and UCHL-1 (CD-45RO) for T-lymphocytes. The sections were also tested by in situ hybridization for EBV mRNA expression, using the EBER-1 probe specific for EBV-1 gene. The 18 lesions included seven malignant LEL, seven benign LEL and four benign lymphoepithelial cysts. All malignant LELs showed a high and diffuse level of epithelial expression of EBV mRNA. Of the 11 benign lesions, only one case showed focal epithelial expression of EBV mRNA. This was a case of benign LEL in an HIV-positive male. All the benign lesions, except that expressing EBV mRNA, showed a T-/B-lymphocyte ratio averaging 2:1. All cases expressing EBV mRNA, including the case of benign LEL in the HIV-positive patient, showed a T-/B-lymphocyte ratio averaging 1:3. Our findings suggest that a T-lymphocyte-mediated immune response may play an essential role in suppressing proliferation of EBV in benign LEL of the parotid gland. This immune mechanism may be significantly disturbed in the malignant lesions, leading to uncontrolled viral replication and carcinogenesis.