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A patient with hemoptysis, anemia, and renal failure.

Article Excerpt
Microscopic polyangiitis is a potentially fatal disease if it is not recognized and treated early. In the case described here, what initially presented as a postinfectious residual cough was actually active pulmonary hemorrhage, severe anemia, and a crescentic glomerulonephritis. Significant improvement was achieved with hemodialysis and aggressive treatment with corticosteroids and cyclophosphamide. This case exemplifies a classic presentation of microscopic polyangiitis and demonstrates the importance of an expeditious diagnostic evaluation and early treatment to prevent rapid deterioration. Early recognition and highly aggressive immunosuppressive treatment achieved significant suppression of the disease.

THE CASE

A 31-year-old man presented to the emergency department with a history of recurrent episodes of hemoptysis for 1 month after an upper respiratory tract infection. Several weeks after the onset of symptoms, he noted fatigue and dyspnea with mild physical exertion. He subsequently noted coffee-ground emesis, several episodes of dark stool, and diarrhea.

The patient sought medical evaluation at a clinic, and penicillin was prescribed. He did not take other medications routinely. He reported a history of alcohol use and intermittent cocaine use for 10 years.

On examination, the patient was afebrile and tachycardic (with a heart rate of 105 beats per minute), and his arterial oxygen saturation on room air was 96%. He appeared generally pale. His oropharynx was erythematous with mild tonsillar hypertrophy. Chest auscultation demonstrated decreased breath sounds with bibasilar rales. The findings from heart, abdomen, and neurological examinations were unremarkable. No purpura, lymphadenopathy, joint tenderness, or synovitis was present.

Laboratory test results revealed a normocytic anemia (hemoglobin, 5.8 g/dL; mean corpuscular volume, 91 fL) without eosinophilia, hyperkalemia (potassium, 6.0 mEq/L), and renal insufficiency (blood urea nitrogen, 96 mg/dL; creatinine, 13.6 mg/dL) with an active urinary sediment (protein more than 300 mg/d; red blood cells, 44 per high-power field). A chest radiograph showed diffuse bilateral patchy infiltrates (Figure 1), which were confirmed by a CT scan.

The patient subsequently underwent bronchoscopy, which showed normal structure and anatomy with old blood near the vocal cords and patchy areas of erythema throughout the bronchial tree (Figure 2). Bronchoalveolar lavage revealed progressively bloody aliquots (Figure 3). Pulmonary function tests showed a carbon monoxide--diffusing capacity of 105% of the predicted value, which is consistent with diffuse pulmonary alveolar hemorrhage.

The diagnosis of a small-vessel vasculitis was entertained, and serological tests were ordered. Antinuclear, anti-Smith, anti-RNP, and antistreptolysin antibody titers and complement levels were all normal. The myeloperoxidase (MPO) antineutrophil cytoplasmic antibody (ANCA) level was elevated at 76 IU (normal, less than 10 IU), but tests for proteinase 3 (PR3)-ANCA and anti--glomerular basement membrane (anti-GBM) antibodies were negative.

Renal...

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