A CASE OF TUBERCULOUS LYMPHADENITIS IN A PERITONEAL DIALYSIS PATIENT WITH DIAGNOSTIC DIFFICULTY

 

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A CASE OF TUBERCULOUS LYMPHADENITIS IN A PERITONEAL DIALYSIS PATIENT WITH DIAGNOSTIC DIFFICULTY

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Takeshi
Tanda
Takeshi Tanda tanda.takeshi.67x@st.kyoto-u.ac.jp Kyoto University Hospital Department of Nephrology Kyoto-shi Japan *
Keiichi Kaneko kekaneko@kuhp.kyoto-u.ac.jp Kyoto University Hospital Department of Nephrology Kyoto-shi Japan -
Mina Kotani minak6097@kuhp.kyoto-u.ac.jp Kyoto University Hospital Department of Nephrology Kyoto-shi Japan -
Shunsuke Kawamura shunkawa@kuhp.kyoto-u.ac.jp Kyoto University Hospital Department of Nephrology Kyoto-shi Japan -
Kan Murata trunk1074@kuhp.kyoto-u.ac.jp Kyoto University Hospital Department of Nephrology Kyoto-shi Japan -
Shinya Yamamoto syamamon@kuhp.kyoto-u.ac.jp Kyoto University Hospital Department of Nephrology Kyoto-shi Japan -
Motoko Yanagita motoy@kuhp.kyoto-u.ac.jp Kyoto University Hospital Department of Nephrology Kyoto-shi Japan -
 
 
 
 
 
 
 
 

Introduction:
Patients with end-stage kidney disease are immunocompromised and have an increased risk of developing tuberculosis (TB). Among dialysis patients, the incidence of TB is particularly high, and in peritoneal dialysis (PD) patients, it has been reported to be approximately seven times higher than in the general population. However, PD patients often present with nonspecific symptoms such as fever and malaise, and extrapulmonary TB is common, making early diagnosis challenging.

Case:
A 78-year-old man with a history of type 2 diabetes mellitus, hypertension, and hyperuricemia was referred to our department for elevated serum creatinine (1.4 mg/dL) detected during a health checkup seven years earlier. He was diagnosed with nephrosclerosis and gouty kidney disease. His renal function decreased gradually, and continuous ambulatory peritoneal dialysis was initiated two years prior. While on peritoneal dialysis, he developed low-grade fever and malaise, which led to hospitalization. Empirical antibiotic therapy was ineffective. Contrast-enhanced CT showed lymphadenopathy in the left hilar, mediastinal, para-aortic, and supraclavicular regions, and PET–CT revealed intense FDG uptake in the left hilar lymph node. Bronchoscopic biopsy showed no malignancy. Serum adenosine deaminase was elevated (63.5 U/L), suggesting TB, but cultures of peritoneal dialysate, sputum, and bronchoalveolar lavage fluid were initially negative for acid-fast bacilli. Because the diagnosis remained uncertain, we considered performing mediastinal lymph node biopsy via mediastinoscopy. However, three weeks later, Mycobacterium tuberculosis was detected in the lavage culture, confirming tuberculous lymphadenitis, and the planned biopsy was deemed unnecessary. Four-drug anti-tuberculosis therapy was initiated, resulting in lymph node shrinkage and improvement of inflammation. However, severe liver injury and thrombocytopenia occurred, requiring temporary discontinuation of all drugs. Gradual reintroduction of isoniazid, rifampicin, and pyrazinamide at reduced doses was tolerated, and treatment was successfully continued.

Discussion:
TB in PD patients is often difficult to diagnose due to the frequent occurrence of extrapulmonary involvement and nonspecific presentation. Multiple diagnostic approaches—including culture of effusions, lavage fluid, and tissue biopsy—should be considered. Furthermore, PD patients are more prone to adverse effects during TB treatment, particularly hepatotoxicity from isoniazid. Previous studies have reported severe liver injury in up to 37.5% of PD patients receiving anti-TB therapy. Because drug toxicity may interrupt treatment completion, careful monitoring during therapy is essential in this population.

 
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