Letter to the Editor Nephron 1995;70:123-124 Ravindra Mittala Sanjiv Saxena* Sandeep Guleriab S.K. Mittala S.K. Agarwala S.C. Tiwaria S.C. Dasha Departments of a Nephrology and b Surgery, AIIMS, New Delhi, India Visceral Leishmaniasis: A Rare Cause of Unexplained Pyrexia in a Renal Allograft Recipient Dear Sir, Visceral leishmaniasis or kala-azar has not been recognised as a common infection in renal allograft recipients. However, im munodeficiency states can facilitate the reac tivation of a dormant illness in infected pa tients or predispose such patients to infec tion in endemic areas. Indeed, following its first description in renal transplant recipi ents in 1979 [1], in recent years more case reports have described such an association [2-5]. In contrast to the non-immunodefi- cient patients, the disease is often more ful minant and poorly responsive to therapy in these high risk patients [3]. We report here a case of visceral leishmaniasis in a renal allo graft recipient who presented with pyrexia of undetermined origin and showed an excel lent response to pentavalent antimonials. A 23-ycar-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 ori gin 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 re vealed a pale, anicteric, febrile patient with no significant peripheral lymphadenopathy. He was normotensivc and the cardiovascu lar and respiratroy systems were normal. Ab dominal examination showed a 2-cm hepa tomegaly 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, plate let 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, scrum bilirubin 0.9 mg/ dl. SGOT 86 IU/ml, SGPT 93 lU/ml and an alkaline phosphatase of 86 IU/ml. The total proteins were 7.1 g/dl with the serum albu min being 3.2 g/dl and the globulins 3.9 g/dl. The rest of serum biochemistry was normal. A routine urinalysis and 24-hour urine ex amination were normal. Radiography of the chest was normal. Peripheral smears for ma larial parasites were negative on three occa sions and repeated blood, urine and throat cultures were sterile. Widal test was negative and showed no increase in titre serially. Se rology for cytomegalovirus was negative for both IgM and IgG antibodies. Mantoux test was negative. Abdominal ultrasonography showed hepatosplenomegaly but no retro peritoneal lymph nodes or masses. The pa tient was initially treated with ciprofloxacin 500 mg b.d. for 2 weeks without response. A repeat empirical course of antimalarials was also administered without success. In view of leucopenia. the patient was restarted on cyclosporine at a dose of 2 mg/kg/day and azathioprine was discontinued. A bone marrow examination was done subsequently and the smears were full of amastigote forms of Leishmania donovcini. Definitive therapy was then instituted in the form of sodium antimony gluconate started in a dose of 8 mg/kg/day in view of deranged LFTs and then stepped up to a dose of 15 mg/kg/day. The patient showed an excellent response with amelioration of toxemia and became afebrile after 7 days of therapy. The therapy was, however, continued for a total of 2 weeks. A repeat bone marrow examina tion done after 4 weeks was reported nega tive for Leishman-Donovan bodies. The pa tient was discharged with normal counts, normal renal parameters and normal LFTs at completion of therapy. The patient has been under follow-up for the last 6 months without recurrence of the disease. Visceral leishmaniasis or kala-azar is en demic in several parts of India with 30 of the 39 districts of Bihar having been identified as currently endemic areas by the WHO [6]. To the best of our knowledge, only 12 cases, including this report, of visceral leishmania sis in renal allograft recipients have been described so far [2-5]. Four of these patients (33.3%) had a fatal outcome mainly due to supcrinfection, most often Pseudomonas septicemia, or disseminated intravascular coagulation [2, 3], and only 8 patients (66.6%) have survived after antiprotozoal therapy [4, 5], The outcome depends on ear ly diagnosis and treatment - which may be delayed because this diagnosis is often not considered in the first place and secondly because of a misleading presentation of the disease in such immunocompromised hosts. The optimum dosage and duration of treat- Dr. Sanjiv Saxcna, Assist. Prof. Department of Nephrology AIIMS New Delhi (India) © 1995 S. Karger AG, Basel 0028-2766/95/0701-0123 $ 8. 00/0