The case is a 32-year-old female patient with a history of cadaveric donor RT in 2006 due to membranoproliferative glomerulonephritis. She received induction therapy with basiliximab and maintenance therapy with tacrolimus, mycophenolate, and deflazacort. She consulted for a 4-week history of diarrheal stools 4 times a day that she controlled with loperamide. In the last week, it was associated with nausea, crampy abdominal pain, and fever. In the last 6 months, she had lost 10 kg and was being managed with oral iron due to normochromic normocytic anemia, with no improvement in hemoglobin levels. She had no other relevant background.
On physical examination, she was tachycardic, afebrile, and normotensive, with abdominal pain in the left flank without signs of peritoneal irritation. Chronic diarrhea and febrile syndrome were considered in an immunosuppressed patient, so studies with fecal microscopy, fecal culture, viral load for CMV, and blood culture were started (Table 1). Due to chronic anemia, studies with folic acid, vitamin B12, ferrokinetic profile, and nutritional profile were extended, confirming iron deficiency anemia.
Renal function was stable with serum creatinine within the patient's usual range. Electrolytes were unaltered, fecal microscopy examination was inflammatory, and cultures were negative. Colonoscopy showed left and transverse colitis with 80% stenosis of the colonic lumen (Figure 1). Biopsies of the compromised segments were taken.
Given the results found in colonoscopy, studies with gastrointestinal film array, CMV viral load in plasma, HIV, and rapid plasma reagin were evaluated, which were negative, as was the Histoplasma urine antigen. Herpes simplex type I and II studies performed in biopsy were negative. Given the suspicion of neoplasia, contrast abdominal tomography was carried out, which showed thickening and enhancement of the walls of the cecum, ascending colon, and hepatic flexure of the colon, with a 4-cm segment with 80% stenosis of the ascending colon lumen. Colon biopsy reported ulcerative component, without identifying microorganisms, dysplasia, or malignancy. Polymerase chain reaction (PCR) for TB and CMV was positive in the biopsy.
The patient was presented at a meeting considering intestinal Mycobacterium tuberculosis (MT) and CMV coinfection. Treatment with valganciclovir for 4 weeks was decided to manage CMV and 4-drug therapy with isoniazid (INH), rifampin (R), pyrazinamide (Z), ethambutol (E), and pyridoxine for GITB management. Tacrolimus dose was adjusted due to drug interaction with rifampin.
During treatment, elevated transaminases (aspartate aminotransferase 414 U/L and alanine transaminase 990 U/L) and uric acid (16 mg/dL) developed. Hepatotoxicity associated with INH was considered, so it was assessed by the pulmonologist who changed INH to moxifloxacin, with improvement in the liver profile. Moxifloxacin, R, and Z were continued for 9 months. The evolution was satisfactory, with the resolution of diarrhea, improvement in anemia, stable renal function (1.48 mg/dL), and weight recovery.