A 44-year-old patient with a history of chronic kidney disease due to IgA nephropathy underwent renal transplant from a related live donor. Subsequently, there was a re-entry into dialysis due to the loss of renal graft function secondary to mixed rejection and BK virus nephropathy. At the time of presentation, the patient had been undergoing thrice-weekly hemodialysis for the past 2 years and reported the onset of evening fevers, approximately 10 kilograms of weight loss over the last 2 months, associated with an increase in abdominal girth, swelling of the lower limbs, and an intermittent non-productive cough. Physical examination revealed cutaneous-mucosal pallor, good respiratory mechanics, bibasal hypoventilation without added sounds. The abdomen was distended and globular, soft, depressible, with ascites, edema of lower limbs, and non-painful erythematous hyperpigmented, desquamative, and crusted lesions on the lower limbs. No axillary or inguinal lymphadenopathy was noted. Laboratory tests, chest X-ray, abdominal ultrasound, serologies for Hepatitis B negative, Hepatitis C negative, HIV negative, negative ANA, negative Anti-DNA, skin biopsy, 0-millimeter Mantoux test, Doppler echocardiogram, chest, abdomen, and pelvic CT scan, blood cultures, direct and sputum cultures were requested.
Concentric left ventricular hypertrophy, mild deterioration of systolic function. Estimated ejection fraction (EF) of 51%.
Paracentesis of ascitic fluid was performed, and the physical-chemical study, direct for acid-fast bacilli (BAAR). Mononuclear predominance was observed in the physical-chemical study of ascitic fluid. Despite daily dialysis sessions, the persistence of ascites led to an exploratory laparotomy with biopsy, direct culture for BAAR, and Xpert. Chest CT reported no significant pulmonary lesions, bilateral laminar pleural effusion predominantly on the left, and pericardial effusion. Abdomen and pelvic CT revealed significant homogeneous free fluid in the abdominal cavity. A skin biopsy indicated leukocytoclastic vasculitis.
Upper gastrointestinal endoscopy revealed a normal esophageal mucosa and no lesions in the esophagus, body, or antrum. The duodenum showed no lesions or pathological findings. Colonoscopy indicated no lesions.
Pathological anatomy findings suggested interstitial histiocytic lymphoplasmacytic infiltration, an active chronic inflammatory process. Culture for acid-fast bacilli returned positive after 45 days. Xpert from the peritoneal biopsy was positive for tuberculosis.
The development of peritoneal
tuberculosis is associated with comorbidities such as immunosuppression, HIV,
chronic kidney disease, and peritoneal dialysis, with no reports in
hemodialysis patients. Approximately 70 percent of patients exhibit symptoms
for more than 4 months before a definitive diagnosis. This delay is partly
attributed to the insidious onset of the disease, and its diagnosis is often
not suspected. Peritoneal infection is typically secondary to hematogenous
dissemination of bacteria from a pulmonary focus, rarely coexisting with active
pulmonary disease.
More than 90% of these
patients present with ascites at the time of diagnosis, with few cases
progressing to an advanced stage known as tuberculous dry peritonitis,
characterized by fibrous adhesions. Tuberculous peritonitis should be
considered in the differential diagnosis of any immunosuppressed patient
presenting with abdominal pain, fever, and weight loss over several weeks.