A 26-year-old male was admitted to the hospital with a 2-week history of cough with expectoration and high-grade fever. He had a history of loss of appetite for ten days. On admission, his blood pressure was 116/76 mm Hg and his body temperature was 37.8 C. Rest of the physical examination was unremarkable, and urine analysis did not show any abnormal findings. The patient's laboratory profile was as follows: hemoglobin: 10.6 g/dL; total leukocyte count: 4,100/mm3; platelet count: 2.6 x 105/mm3; erythrocyte sedimentation rate (ESR): 58 mm/hr; serum creatinine: 0.86 mg/dL; sodium: 138 mEq/L; potassium: 3.7 mEq/L; and serum albumin: 4.2 g/dL. The chest X-ray showed dense homogenous opacity in right upper zone area of lung. PPD (purified protein derivative of tuberculin) skin test showed a positive reaction, and sputum smear for acid-fast bacilli was found to be positive. On the basis of clinical symptoms, high ESR, positive PPD skin test, positive sputum smear for acid-fast bacilli, and chest X-ray findings, the diagnosis of pulmonary tuberculosis was made. The antituberculosis treatment was started with rifampicin 450 mg/day, isoniazid 300 mg/day, ethambutol hydrochloride 800 mg/day, and pyrazinamide 1000 mg/day.
After one month of daily treatment, the patient became sputum smear negative for acid-fast bacilli, but he developed sudden onset swelling whole over the body. The patient's laboratory profile at that time was as follows: hemoglobin: 12.9 g/dL; total leukocyte count: 9,700/mm3; platelet count: 2.6 x 105/mm3; urinary protein: 3+; urinary sugar: 0; urine microscopy:white blood cell count: 2-3/high-power field; red blood cell count: 0-1/high-power field; urinary pH: 6.2; urinary albumin: 3+; serum albumin: 2.7 g/dL; serum sodium: 136.4 mEq/L; serum potassium: 4.4 mEq/L; blood urea: 36 mg/dL; serum creatinine: 0.82 mg/dL; serum cholesterol: 296 mg/dl; serum glutamic oxaloacetic transaminase (SGOT): 32 U/L; serum glutamic pyruvic transaminase (SGPT): 36 U/L; serum bilirubin total: 0.9 mg/dL; C3: 106.0 mg/dL (normal range: 90-180); C4: 18 mg/dL (normal range: 10-40); serum antinuclear antibody: negative; serum antistreptolysin O titer (ASO titer): <110 IU/mL; cytoplasmic antineutrophil cytoplasmic antibody: negative; perinuclear antineutrophil cytoplasmic antibody: negative; HIV I and II: negative; HBsAg: negative; and anti-HCV: negative. A 24-hour urinary protein value was 10.8 grams/day. Ultrasonography abdomen showed bilateral normal size kidneys with normal echogenicity. A renal biopsy showed nonproliferative glomerulopathy (22 glomeruli) (Figure 1). Tubular atrophy involved less than 10% of the sampled cortex. Tubules showed focally prominent cytoplasmic vacuolar changes, and the arteries sampled appeared unremarkable. Direct immunofluorescence did not show significant glomerular immune deposits. Renal electron microscopy showed diffuse effacement of visceral epithelial cell foot processes (Figure 2). Rifampicin-induced secondary minimal change disease was suspected, and the culprit drug rifampicin was stopped immediately. The other antitubercular drugs were continued with the addition of levofloxacin 500 mg/day. The proteinuria started to decline, and 24-hour urinary protein was 1.2 grams/day after two weeks of stopping of rifampicin. After 30 days of cessation of rifampicin, proteinuria was undetectable in 24-hour urinary samples, and serum albumin and serum cholesterol were found to be normal. The pulmonary tuberculosis was well managed by isoniazid, ethambutol hydrochloride, and levofloxacin, and there was no recurrence of proteinuria.