A 30-year-old renal transplant recipient presented with fever of 2-month duration in August 2008. Five years back, he had undergone renal transplantation with his sister as donor. His basic kidney disease was unknown and he was on triple immunosuppression with cyclosporine (CsA), azathioprine (AZA) and prednisolone. His baseline serum creatinine was 1.2 mg/dl. In addition to the fever, he also complained of malaise and weight loss of 5 kg during the last 2 months. He had no history of cough, expectoration, loose stools, dysuria or increased urinary frequency. He had no history of tuberculosis in the past.
On examination, he was febrile and had pallor but there were no palpable lymph nodes. His blood pressure was 130/90 mmHg. Examination of the various organ systems was essentially unremarkable.
His hemoglobin was 9.2 g/dl, total leukocyte count 2400/mm3, platelet count of 160 x 103/ mm3, erythrocyte sedimentation rate 30 mm/1st hour, serum creatinine was 1 mg/dl, sodium 142 mEq/L, potassium 4.7 mEq/L, serum bilirubin 0.73 mg/dl, aspartate aminotransferase 40 IU/L, alanine aminotransferase 26 IU/L, alkaline phosphatase 446 IU/L, serum total protein 7.5 g/dl, serum albumin 3.4 g/dl and the fasting serum glucose was 104 mg/dl. Ultrasonography of the abdomen revealed 5 x 6 cm hypo-echoic lesion in segment V of the liver. A contrast- enhanced computed tomographic scan of the thorax and abdomen revealed multiple, confluent hypodense lesions in the liver, spleen, the renal allograft [Figure 1] and prostate [Figure 2], along with multiple enlarged lymph nodes in the mesentery with central necrosis. The prostate showed multiple air specks also. The high-resolution computed tomography of lungs showed typical miliary pattern. Fine-needle aspiration cytology from the lesion in the liver showed numerous acid-fast bacilli; acid- fast bacilli were also demonstrated in the overnight urine sample. A bone marrow examination, which was performed in view of persistent leucopenia, showed hypocellularity with megaloblastosis, but there were no acid-fast bacilli or granuloma seen. HBsAg (hepatitis B surface antigen) and anti-HCV (hepatitis C virus) antibody were negative, HIV serology was non-reactive and his serum was negative for Cytomegalovirus DNA. Urine cultures performed repeatedly were sterile despite persistent pyuria.
He was started on 4-drug anti-tuberculous therapy (ATT) with isoniazid, ciprofloxacin, ethmbutol and pyrazinamide. AZA was stopped in view of the severe leucopenia. The cyclosporine dose was also reduced. He became afebrile by the end of first week of ATT. He also required treatment with granulocyte colony-stimulating factor as the leucopenia worsened further despite discontinuation of AZA.