A 27-year-old man with end-stage kidney disease from chronic glomerulonephritis received a renal allograft from his mother in 2005 using prednisolone, cyclosporine and azathioprine, without induction therapy. During the immediate post transplant period, he received three intravenous pulses of methylprednisolone 1 g each daily for acute cellular rejection. He did not develop major infections till the current episode. His weight was 58 kg. He had stable graft function, with serum creatinine at 1.6 mg/dl and was on prednisolone 10 mg/d, azathioprine 100 mg/d and cyclosporine 175 mg/d, with the trough (C0) and 2-hour (C2) cyclosporine levels being 368 and 1280 ng/ml, respectively, at 6 months after transplantation.
Three years after transplantation, he presented to us with 4 months history of fever, weight loss of 16 kg in 4 months, episodic small volume diarrhea and diffuse abdominal pain with occasional hematochezia. He did not have pulmonary or other gastrointestinal symptoms. He discontinued cyclosporine 4 months prior to visiting our center. At presentation, he was on prednisolone (10 mg/d) and azathioprine (100 mg/d). On examination, his weight was 38 kg, and pulse rate, blood pressure, respiratory rate were normal. He was pale but did not have icterus or peripheral lymphadenopathy or allograft tenderness. He had a diffuse, ill-defined, firm, tender mass (9 x 7 cm) in the right hypochondrium. There was no hepatosplenomegaly or ascites.
Laboratory investigations revealed anemia (hemoglobin of 6.7 g/dl), a total leukocyte count of 4200/mm3, a normal platelet count and serum albumin of 2.2 g/dl. He had renal allograft dysfunction (serum creatinine of 3.1 mg/dl) with normal electrolyte profile and liver enzymes. His chest radiograph revealed an ill-defined minimal haziness in the right upper and midzones with minimal pleural effusion. Ultrasonogram of abdomen showed an intussusception mass measuring 7.1 x 5.0 x 10.1 cm in the right hypochondrium with a few enlarged mesenteric nodes and fat within and adjacent to it [Figure 1a]. The renal allograft appeared normal. Computed tomogram (CT) scan of abdomen with rectal contrast revealed an ileocolic intussusception up to the hepatic flexure with multiple enlarged mesenteric nodes and mesenteric fat pulled into it [Figure 1b]. The ascending colon was thick. The para-aortic, mesenteric and para-iliac nodes were enlarged and showed central necrosis.
The patient underwent an emergency exploratory laparotomy with resection of the ileocolic intussusception, the adjacent ascending colon and terminal ileum [Figure 2a]. Histopathological examination of the ileocolic intussusception revealed fragments of a lymph node with extensive caseation necrosis and many acid-fast bacilli (AFB). The proximal polypoidal lesion of the intussusceptum and the mucosal ulcerations of the intussuscepient colonic segment revealed dense inflammatory infiltrates of lymphocytes and plasma cells, along with microabscesses in the submucosa and lamina propria, transmural granulomas with epitheloid histiocytes, lymphocytes; Langhans type multinucleated giant cells and central foci of caseation [Figure 2b and d]. Long, curved and beaded AFB, morphologically typical of Mycobacterium tuberculosis (MTB), were detected in all the above-mentioned lesions [Figure 2c].
On the first postoperative day, the patient received hydrocortisone 100 mg thrice daily, but azathioprine was discontinued due to leukopenia (WBC count 1900/mm3). He received granulocyte colony stimulating factor for leukopenia. On the second postoperative day, he was weaned off mechanical ventilation. On the fourth postoperative day, he received ATT with isoniazid 300 mg/d, rifampicin 450 mg/d, pyrazinamide 750 mg/d and ethambutol 400 mg/d. On the fifth postoperative day, 36 hours after starting ATT, he developed tachycardia, tachypnea, hypotension, oliguria and worsening of pulmonary oxygenation [partial pressure to inspired fraction of oxygen ratio (P-F ratio)]. The chest radiograph revealed worsening of the preexisting haziness. However, there was no bacteremia or evidence of invasive fungal infection.The total leukocyte count had remained about 4500 cells/mm3 during this period. His condition subsequently worsened, and he received broad-spectrum antibiotics (piperacillin with tazobactam) while routine cultures remained sterile. A tracheal aspirate showed numerous AFB morphologically typical of MTB, though there was no growth in culture. In addition, tracheal aspirate grew mixture of non-fermenting gram negative bacilli and Candida glabrata, which were probably contaminants. He continued to develop worsening features of a systemic inflammatory response syndrome, lung infiltrates, and disseminated intravascular coagulation. Steroids were continued, antibiotics were changed empirically to meropenem with teicoplanin and liposomal amphotericin B. The patient died on the 11th postoperative day. The next of kin declined post-mortem examination.