Case Presentation: A 49 year-old woman with end stage renal disease on peritoneal dialysis (PD) for the past year, presented with progressively worsening abdominal pain, fevers, and nausea. This was her second presentation as she had been treated with antibiotics for presumed culture-negative PD-catheter-associated bacterial peritonitis three weeks earlier without improvement.
Admission vital signs and physical exam were unremarkable except for a heart rate of 138 beats per minute and an exquisitely tender, distended abdomen. Her PD catheter site appeared normal. She had a normal white blood cell (WBC) count, elevated phosphorus of 6.7mg/dL, and elevated calcium of 10.5mg/dL, correcting to 12.0mg/dL (albumin 2.1g/dL). Peritoneal fluid revealed 106 WBCs/mm3 (38% lymphocytes, 31% neutrophils) with negative bacterial cultures. CT scan showed a diffusely thickened peritoneum without abdominal lymphadenopathy. Vancomycin and cefepime were started for likely treatment failure of bacterial peritonitis.
Her abdominal pain and fevers persisted despite antibiotics; bacterial, fungal, and acid-fast bacilli (AFB) cultures remained negative. Her hypercalcemia, first attributed to tertiary hyperparathyroidism, raised concern for malignancy or atypical infections given her continued pain. Work-up of her hypercalcemia showed low PTH, PTHrP, and 25-OH Vitamin D, but high 1,25-OH Vitamin D, suggesting lymphoma or a granulomatous process. Recent quantiferon gold was indeterminate. Ascitic adenosine deaminase (ADA) was elevated. She underwent peritoneal biopsy showing necrotizing granulomas. She started rifampin, isoniazid, pyrazinamide and ethambutol (RIPE) therapy for presumed TB peritonitis and her ascitic AFB cultures grew Mycobacterium tuberculosis (Mtb) three weeks later.
Discussion: Hypercalcemia is common in hospitalized patients and typically caused by primary hyperparathyroidism, malignancy, or chronic kidney disease, but should always be investigated to determine the precise etiology. Full laboratory evaluation in this case revealed a 1,25-OH Vitamin-D-driven hypercalcemia and prompted work-up for TB peritonitis given her protracted symptoms.
Despite improving diagnostic tools, TB peritonitis remains an elusive diagnosis. Presenting symptoms are non-specific and can mimic bacterial peritonitis, chemical peritonitis, and peritoneal carcinomatosis. Standard volumes of 10-50mLs ascitic fluid normally yield negative AFB cultures. When suspected, further work-up for TB peritonitis can include ascitic ADA, Mtb PCR, larger volume of ascitic fluid cultures (ideally 1 liter), and peritoneal biopsy. Most patients with latent Mtb infection experience reactivation within their first year of dialysis. Patients undergoing PD are more likely than hemodialysis patients to have reactivation TB peritonitis, which scientists suspect is due to PD hindering the local cellular immunity of the peritoneum.
Conclusions: Hospitalists should always pursue a complete workup of hypercalcemia to identify an etiology. TB peritonitis is difficult to diagnose, complicated by slow growing, and often negative, cultures. A 1,25-OH Vitamin-D-driven hypercalcemia in patients undergoing peritoneal dialysis should prompt hospitalists to consider tuberculous peritonitis earlier, expedite diagnosis, and consider empiric treatment while awaiting AFB cultures.