A 51-year-old Spanish-speaking male with hypertension and diabetes mellitus complicated by end-stage kidney disease presented to the emergency department for routine hemodialysis with subacute abdominal swelling and discomfort. He endorsed night sweats, 10-lb weight loss, and intermittent diarrhea and constipation over a 6-month duration. He denied shortness of breath, cough, bruising, and vomiting. The patient immigrated from Mexico 24 years earlier and had no exposure to the prison system or housing instability. He was uninsured and relied upon a county hospital compassionate dialysis session twice weekly on Wednesdays and Saturdays through a right subclavian tunneled dialysis catheter.
Notably, the patient's workup had begun in the outpatient setting, five months before his current presentation, when he sought care for the above symptoms, in combination with bilateral pleural effusions, chronic hypoxic respiratory failure (on 1-2 L home oxygen), and cervical lymphadenopathy that were concerning for malignancy. However, the workup had been nondiagnostic. Prior pleural fluid analysis was consistent with an exudative and lymphocytic process with negative acid-fast bacilli (AFB) cultures and negative cytology. Fine needle aspiration of the known cervical lymphadenopathy revealed granulomatous inflammation and both negative cytology and flow cytometry. In the month prior to presentation, he had developed new onset ascites that had been drained and attributed to "nephrogenic ascites" that was attributed to chronic underdialysis given his twice weekly compassionate dialysis and repeated presentations with volume overload. He was admitted to the medicine service for routine dialysis and further workup of ascites.
On admission, his blood pressure was 160/60 mmHg and his oxygen saturation was 99% on room air. His exam on admission was notable for temporal wasting, anicteric sclera, a moderately distended abdomen with shifting dullness, painless and mobile cervical lymphadenopathy, and decreased basilar breath sounds. Pertinent labs included potassium 5.6 mEq/L, BUN 84 mg/dL, phosphorus 8.3 mg/dL, Cr 10.2 mg/dL, (GFR mL/min/1.73 m2), Hgb 10.1, alkaline phosphatase 585 U/L, calcium 13 mg/dL (increased from 8.7 mg/dL six months prior), parathyroid hormone 12 pg/mL, and vitamin D1, 25 hydroxylase 100 ng/mL. Admission EKG showed left ventricular hypertrophy but did not show peaked T waves or any abnormal intervals. Chest x-ray showed prominent pleural effusions. Transthoracic echocardiogram performed 4 months earlier showed normal left ventricular systolic function (ejection fraction 60-65%), grade II diastolic function, with increased left atrial pressure, and normal right ventricular systolic function and no pericardial effusion. Computed tomography of the chest was notable for multistation mediastinal lymphadenopathy, bilateral upper lobe predominant perilymphatic lung nodules, and bilateral pleural effusions with pleural thickening, suggestive of pulmonary sarcoidosis with a differential of atypical mycobacterial infections. Radiology noted that nodularity and hyperenhancing lymphadenopathy that was unusual for disseminated mycobacterial tuberculosis or histoplasmosis given lack of miliary pattern. Computed tomography of the abdomen and pelvis demonstrated anasarca, large volume abdominopelvic ascites with peritoneal thickening, and nodularity throughout the omentum (Figure 1(a)). MRI abdomen/pelvis with contrast showed enhancing soft tissue thickening throughout the greater omentum (Figures 1(b) and 1(c)) and in their impression suggested the possibility of malignancy with peritoneal carcinomatosis with recommendation for tissue sampling.
Based upon this patient's ongoing outpatient workup and new imaging findings, there was skepticism that the ascites was solely attributable to inadequate dialysis. For both diagnostic and therapeutic purposes, paracentesis was performed. The ascitic fluid analysis revealed a serum ascites albumin gradient of less than 1.1 gm/dL, which was not consistent with an etiology secondary to elevated hydrostatic pressure. Additionally, fluid studies indicated an elevated adenosine deaminase level of 32.6 U/L but a negative AFB stain. Serum interferon gamma release assay was positive. Core biopsy of cervical lymph node revealed granulomatous inflammation with central necrosis and also negative AFB stain. Bronchoscopy was unrevealing. AFB stain and MTB PCR were positive on sputum sample, eventually growing pan-sensitiveMycobacterium tuberculosis. Patient was initiated on RIPE therapy (i.e., rifamycin, isoniazid, pyrazinamide, and ethambutol) empirically after bronchoscopy was complete. Given the patient's constellation of symptoms, hypercalcemia with evidence of granulomatous disease, and imaging findings of omental caking and pulmonary disease, a final diagnosis of disseminated tuberculosis was made with confirmed sputum sample.