Case Report: Nephrotic syndrome with minimal change disease during anti-tuberculosis treatment and tiopronin use

Hepatoprotective agents are often added during prolonged anti-tuberculosis (anti-TB) therapy, and medication-associated nephrotic syndrome may be under-recognized.

A 31-year-old man with pulmonary tuberculosis received long-term anti-TB therapy (rifapentine, isoniazid, and ethambutol) and continuous tiopronin (0.2 g three times daily). He developed edema, foamy urine, and oliguria. Pre-admission tests showed proteinuria (3+), serum albumin 19.6 g/L, and serum creatinine 161 μmol/L. On admission, urine protein was 4+, serum albumin 20.6 g/L, serum creatinine 142.9 μmol/L, and estimated glomerular filtration rate (eGFR) 58.86 mL/min, with hyperlipidemia. Kidney biopsy confirmed minimal change disease (MCD).

All anti-TB drugs and tiopronin were discontinued, and tacrolimus was initiated after biopsy. Anti-TB therapy was reintroduced as isoniazid monotherapy. Renal function improved rapidly (serum creatinine 55 μmol/L; eGFR 128.1 mL/min at discharge), and dipstick proteinuria became negative on short-term follow-up. The tacrolimus trough concentration was 3.6 ng/mL.

The improvement after withdrawal of multiple suspected agents and continued recovery after reintroduction of isoniazid alone support a drug-associated etiology, but do not allow definitive attribution to a single causative drug. Routine renal monitoring should accompany hepatoprotective add-on therapy during anti-TB treatment.