Post-transplant lymphoproliferative disorder (PTLD) is a serious complication of solid organ transplantation. It occurs in 1% of kidney transplants. More than 80% of the incidences of PTLD occur within the first year after transplant. The most common risk factors for PTLD include Epstein-Barr virus (EBV) infection and the degree and type of immunosuppression. 1,2 We report a case of a patient who presented with PTLD with severe acute renal failure 17 years after kidney transplantation. He had an excellent response to the chemotherapy regimen and remained in remission for 6 months, before he was found to have recurrence of the disease in his cervical lymph nodes. The patient refused further chemotherapy and died after a month with normal renal function.
Case ReportA 63-year-old male farmer with a history of end-stage renal disease secondary to poststreptococcal glomerulonephritis received a renal transplant of a kidney from a living related donor, his daughter, in 1988. The patient was on oral prednisone 5 mg daily and cyclosporine 125 mg twice daily for maintenance immunosuppressive therapy. His graft function was stable, with a serum creatinine of 1.1 mg/dL. Seventeen years after transplantation, he presented to his primary care physician with low back pain, generalized fatigue, and nausea. He received oxycodone and acetaminophen/hydrocodone for presumed muscle spasm. The patient noticed right groin pain after a few days. His serum creatinine concentration had increased from 1.1 mg/dL, 7 months earlier, to 6.4 mg/dL. The patient had not received NSAIDs or ACE inhibitors. The patient received intravenous fluid for presumed dehydration. There was no improvement in renal function, and the patient was transferred to our hospital for further evaluation. His cyclosporine level was 162 ng/mL on admission and gradually trended down as it was held.The patient underwent acute hemodialysis. A kidney biopsy was performed to rule out acute allograft rejection. The biopsy revealed a dense cellular infiltrate that spread apart residual renal tubules and glomeruli. The infiltrate was relatively monomorphic and was composed predominantly of large atypical lymphoid cells with irregular nuclei, variable nucleoli, frequent mitoses, and variable quantities of amphophilic cytoplasm ( Figure 1A).Immunohistochemical staining was positive for CD20, CD79a, and Bcl-2 and negative for Kappa, Lambda, and Bcl-6 ( Figure 1B, C). The histology and immunohistochemical studies were consistent with the diagnosis of monomorphic PTLD-large B-cell lymphoma. Fluorescence in situ hybridization (FISH) revealed that the vast majority of cells were of male origin, consistent with recipient-derived tumor cells.Serum antibody titers to EBV capsid (IgG) was positive at 10.3, and to EBV early D Ag was positive at 3.41. EBV Nucl AG IgG and EBV capsid IgM were negative. EBV PCR was positive. CMV PCR and antigenemia were not tested for. Bone marrow aspiration and biopsy did not show any evidence of malignant lymphoma. A staging CT scan of the neck, chest, and ...