A Rare Case of Hydralazine-Induced Diffuse Alveolar Hemorrhage

Hydralazine-induced anti-neutrophil cytoplasmic antibody (ANCA) vasculitis may occur any time after hydralazine initiation. General internists should recognize diffuse alveolar hemorrhage (DAH) as a rare complication of this condition, as early treatment reduces the associated high risk of mortality. We describe the case of an 82-year-old female with diastolic heart failure who presented with a one-month history of worsening dyspnea on exertion and a one-week history of scant hemoptysis and fatigue. Her medications included aspirin and hydralazine. She was hypoxic with bilateral expiratory wheezes on exam. Labs showed new anemia, elevated creatinine, proteinuria, and hematuria. Chest computed tomography showed asymmetric bilateral upper lobe ground-glass attenuation superimposed on interlobular septal thickening and intralobular lines. Further testing showed anti-nuclear antibody, positive ANCA, perinuclear ANCA (p-ANCA), and anti-myeloperoxidase ANCA (anti-MPO-ANCA). Renal biopsy revealed MPO-ANCA, pauci-immune, necrotizing, and crescentic glomerulonephritis. She was diagnosed with DAH secondary to hydralazine-induced ANCA-associated vasculitis (AAV). Hydralazine is an anti-hypertensive medication with known potential for autoimmune reactions. Of these, AAV is a rare sequela mediated by anti-MPO and most commonly affects the kidneys. In rare circumstances, patients with AAV can develop pulmonary-renal syndrome, resulting in both glomerulonephritis and DAH with an associated high risk of mortality. Diagnosis requires a high index of suspicion in patients with acute kidney injury of unclear etiology. Early diagnosis through immune work-up and kidney biopsy should be pursued, as prompt recognition of the vasculitis, cessation of hydralazine, immunosuppression, and early plasma exchange are essential to an improved prognosis.