A 41-year-old man was admitted to our hospital because of generalized purpura and productive cough. He was well until 2 months earlier when he developed productive cough with whitish mucoid sputum and exertional dyspnea. At that time, he was admitted to a local hospital and treated with antituberculous agents for pulmonary tuberculosis confirmed by positive sputum for acid-fast bacilli (AFB). Forty five days before entry, he noticed generalized purpura, more prominent in the lower extremities, and mild pretibial edema. Ten days before admission, high fever and generalized weakness occurred in spite of antituberculosis medication.
He was a government employee and nonsmoker. His past medical history was noncontributory. There was no history of previous nausea, vomiting, abdominal pain, constipation, diarrhea, weight loss and arthralgia.
On examination, he was febrile state, temperature 38.1  C, with a blood pressure of 130/90mmHg, a respiratory rate of 20 per minute, and a heart rate of 112 beats per minute. Multiple, 0.5 x 0.5cm sized, nontender cervical lymph nodes were detected. The conjunctivae were pale. Coarse breathing sounds were heard over the both lung with rale. His bowel sounds were normal and there was no evidence of hepatosplenomegaly. Numerous nontender palpable purpura, located primarily on the lower extremities, were present with pretibial pitting edema (Fig. 1).
The chest roentgenogram taken on admission revealed diffuse scattered, ill defined nodules in entire both lung fields and patchy and confluent density in both upper lungs(Fig. 2). Abdominal ultrasonogram showed increased echoes of renal parenchyme with upper normal size. Others were not remarkable.
The hemoglobin was 9.0g/dl, with 2.8% reticulocytes. The hematocrit was 27.2%. The white blood cell count was 14.3 x 109/L, with a differential of 75% neutrophils, 20% lymphocytes, 3% monocytes, 1% eosinophil and 1% atypical lymphocyte. Wintrobe erythrocyte sedimentation rate was 65 mm/hr(corrected 18 mm/hr). The platelet count was 438 x 109/L. The antiplatelet antibody was negative. The prothrombin time and partial thromboplastin time were within normal limits. Blood chemistry revealed total serum protein 5.8 g/dl, albumin 1.7 g/dl, AST 65 U/L, ALT 23 U/L, triglyceride 109 mg/dl, BUN 22.5 mg/dl, creatinine 1.5 mg/dl, calcium 7.6 mg/dl and phosphate 5.1 mg/dl with normal serum electrolyte. The serum Ig A was 640 mg/dl, Ig G 2020 mg/dl, Ig M 150 mg/dl and Ig E 831 IU/ml. The serum C3, C4 were 162, 37.8 mg/dl, respectively. The urinalysis was reported as showing 300 mg/dl of proteinuria, 20-25 red blood cells, 3-5 white cells per high-power field and WBC cast. Sixty-five percent of the red cells were dysmorphic. In a 24-hour specimen of urine, protein was 6930 mg, creatinine 693 mg. A serum protein electrophoresis revealed hypoalbuminemia with increased gamma globulin fraction and urine electrophoresis showed protein losing pattern. Stool specimen gave a negative test for occult blood. The tests for antistreptolysin O titer, ANA, LE cell, VDRL, hepatitis B surface antigen and antibody and rheumatoid factor were all negative.
Cultures of blood remained sterile. The arterial blood gas showed pH 7.37, PCO2 32.4 mmHg. PO2 71.6 mmHg, HCO3 18.9 mmol/L. The pulmonary function studies showed that FEV1 was 2.04 L(62% predicted). Three separate smears of sputum for AFB were negative. The antituberculous chemotherapy was begun with isoniazid (300 mg), ethambutol (800 mg), rifampin (450 mg) and pyrazinamide (1.5 g), all once daily with pyridoxine. A punch biopsy specimen of the palpable purpuric lesions on the posterior aspect of the leg was consistent with the diagnosis of "leukocytoclastic vasculitis" (Fig. 3). The hospital course was complicated by continued hematuria and proteinuria. The skin lesions slowly resolved by antituberculous agents. The patient was discharged nineteen days later and then readmitted five weeks later for renal biopsy.
On readmission, clinical signs were improved and the pulmonary lesions on chest X-ray film were slightly cleared. Renal biopsy was performed. Light microscopy demonstrated mesangial cell hyperplasia and widening of mesangial matrix. There were fibrous crescents associated with adhesion of Bowman's capsule (Fig. 4). There was the evidence of interstitial chronic granulomatous inflammation with caseous necrosis, with moderate fibrosis, lymphoplasmacytic infiltration, compatible with renal involvement of tuberculosis(Fig. 5). Immunofluorescent findings were strong nodular mesangial Ig A deposit with trace granular Ig G deposition along peripheral capillary loops and perivascular C3 deposit(Fig. 6).
Thereafter, antituberculous drugs were administered for 12 months. He completely recovered from the pulmonary and renal manifestations and remained symptom free in 24 months after antituberculous drugs started.