[Lymphoproliferative syndrome induced by Epstein-Barr virus after kidney transplantation: value of genotypic analysis].

Forty-six days after renal transplantation for inborn tubulointerstitial nephropathy, an 18-year-old man was rehospitalized for renal failure with creatinine at 200 mumol/l. There was no sign of infection and ciclosporin level was within therapeutic range. Transplant biopsy showed minor interstitial infiltration with mononucleated cells. Methylprednisolone by 10 mg/kg/d bolus did not improve renal function and OKT3 5 mg/d was substituted for ciclosporin but had to be stopped on day 8 because of a severe infectious syndrome. The patient developed fever (39 degrees C), erythemato-pultaceous pharyngitis followed by major multiple lymph node and spleen enlargement. The diagnosis of primary Epstein-Barr infection was confirmed serologically. Histology of a submaxillary lymph node reported monomorphic immunoblastic lymphoproliferation. Immunologic phenotyping showed CD19, CD20 and CD22 surface antigens characteristic of B cells and in situ Epstein-Barr hybridization was positive in 100% of the cells. Southern Blot showed an oligoclonal pattern. Ciclosporin and azathioprin were stopped and the patient was treated with corticosteroids (15 mg/d) and aciclovir given orally (3.2 g/d) for 3 months. Outcome at six months was favorable with normalization of the renal function and complete regression of the infectious syndrome. This case demonstrated the importance of molecular biology techniques for virologic and genotypic assessment of lymphomatous proliferation allowing positive aetiologic diagnosis.