Visceral Leishmaniasis: A Rare Cause of Unexplained Pyrexia in a Renal Allograft Recipient

Dr. Sanjiv Saxena, Assist. Prof., Department of Nephrology, AIIMS, New Delhi (India) Dear Sir, Visceral leishmaniasis or kala-azar has not been recognised as a common infection in renal allograft recipients. However, immunodeficiency states can facilitate the reactivation of a dormant illness in infected patients or predispose such patients to infection in endemic areas. Indeed, following its first description in renal transplant recipients in 1979 [1], in recent years more case reports have described such an association [2-5]. In contrast to the nonimmunodefi-cient patients, the disease is often more fulminant and poorly responsive to therapy in these high risk patients [3]. We report here a case of visceral leishmaniasis in a renal allograft recipient who presented with pyrexia of undetermined origin and showed an excellent response to pentavalent antimonials. A 23-year-old young male, resident of Bihar, India, underwent a one-haplotype-matched live related renal transplantation for Alport’s syndrome with end stage renal disease at our centre in December 1992. Immunosuppression given comprised three drugs – azathioprine, prednisolone and cy-closporine, with a gradual tapering off from cyclosporine from 3 months onwards so as to be completely weaned off by 9 months. The early posttransplant period was uneventful. In June 1993 the patient was admitted for evaluation of his pyrexia of unknown origin of 3 weeks duration. The fever was high grade and remittent in nature without any localising symptoms. He had received an empirical course of antimalarials twice (chloroquine followed by a sulphamethoxa-zole and pyrimethamine combination) and also broad-spectrum antibiotics (ampicillin and norfloxacin) for his pyrexia in Bihar without response. Physical examination revealed a pale, anicteric, febrile patient with no significant peripheral lymphadenopathy. He was normotensive and the cardiovascular and respiratroy systems were normal. Abdominal examination showed a 2-cm hepatomegaly and a firm 3-cm splenomegaly with the allograft being normal and non-tender. Investigations on admission revealed a haemoglobin of 6.4 g/dl, reticulocyte count 1%, total leucocyte count 3,200/mm3, platelet count of 90,000/mm3 and ESR of 33 mm in the 1st h. Blood urea was 30 mg/dl, serum creatinine 1 mg/dl, serum bilirubin 0.9 mg/ dl, SGOT 86