Mycobacterium kansasii is an exceptionally rare cause of peritoneal dialysis (PD)-related peritonitis and may present with subtle, indolent features that delay recognition. This case illustrates how “silent” atypical peritonitis can be unmasked by pairing contrast-enhanced computed tomography (CT) with CT peritoneography: the former identified nodular biopsy targets, while the latter revealed loculated dialysate flow and failure of free intraperitoneal circulation. A 20-year-old male had received automated PD for 3 years and was being evaluated for combined heart–kidney transplantation because of severe cardiomyopathy. He presented with vague abdominal discomfort, declining ultrafiltration, mild pedal edema, and weight loss. PD effluent (PDE) showed mononuclear-predominant leukocytosis (49–150 cells/µL), but repeated PDE cultures, AFB staining, and molecular testing were negative. Contrast-enhanced CT revealed multiple peritoneal nodules and omental stranding; CT peritoneography exposed a trapped contrast-containing pocket, providing functional evidence of impaired dialysate circulation. Ultrasound-guided biopsy showed necrotizing granulomatous inflammation, and tissue culture subsequently grew M. kansasii with rifampicin resistance. Because the isolate was also resistant to moxifloxacin and ciprofloxacin, fluoroquinolone-based therapy was avoided. Guided by susceptibility testing, we treated him with isoniazid, azithromycin, ethambutol, and amikacin, and the PD catheter was removed for refractory atypical mycobacterial peritonitis with progressive catheter dysfunction, prompting transition to hemodialysis. Symptoms and inflammatory markers resolved within 6 weeks; however, antimycobacterial therapy was curtailed at 165–179 days when the patient sustained an out-of-hospital sudden cardiac arrest of undetermined cause, in the setting of his severe underlying cardiomyopathy. This case adds to the limited literature on M. kansasii PD peritonitis and describes an imaging-guided diagnostic pathway in which contrast-enhanced CT localized peritoneal lesions, CT peritoneography demonstrated impaired dialysate circulation, and targeted biopsy enabled tissue diagnosis. Susceptibility-guided therapy and catheter removal were followed by clinical control of the infection, although definitive cure could not be established because follow-up ended with the patient’s death. As a single case, these observations are hypothesis-generating and should not be interpreted as establishing diagnostic criteria or standard management.
Lertsuttimetta et al. (Mon,) studied this question.