A 62-year-old white woman presented to the ED with progressive dyspnea and a nonproductive cough unresponsive to oral antibiotics for 1 month. Six years before presentation, she underwent deceased-donor renal transplantation for end-stage renal disease secondary to analgesic abuse. She was treated with cyclosporine and mycophenolate mofetil until 1 year before presentation, when cyclosporine was replaced by everolimus because of difficult-to-control hypertension. The patient had a history of gastric ulcer, parathyroidectomy, percutaneous transluminal angioplasty of the left iliac artery to dilate a stenosis proximal of the allograft kidney, and diabetes mellitus posttransplant. Concomitant medications were bisoprolol, hydrochlorothiazide, moxonidine, amlodipine, metformin, gliquidone, molsidomine, alfacalcidol, venlafaxine, tramadol, lormetazepam, diclofenac, mirtazapine, and aspirin. At presentation, blood pressure was 120/60 mm Hg, heart rate was regular at 120 beats/min, respiratory rate was 28 breaths/min, and temperature was 37.4°C. Auscultation revealed diffuse inspiratory crackles and expiratory wheezing over both lungs. The patient had cyanotic lips and pedal edema, without clubbing, rash, or purpura. Laboratory testing revealed a C-reactive protein of 154 mg/L (normal < 5), a lactate dehydrogenase level of 744 U/L (normal 240-480), a hemoglobin of 10.0 g/dL (normal 11.5-16.5), a platelet count of 218 109/L (normal 140-440), normal coagulation parameters, a serum creatinine of 1.2 mg/dL (normal 0.5-0.9), and a serum urea nitrogen of 56 mg/dL (normal 10-50). Antinuclear factor, antineutrophil cytoplasmic antibodies, and antiglomerular basement membrane antibodies tests were negative. The everolimus through level was 3.3 ng/mL. Chest radiographs showed bilateral diffuse alveolar infiltrates, and chest CT revealed bilateral patchy airspace opacities with air-bronchograms, diffuse ground-glass opacities, septal thickening, and bilateral pleural effusions. A transthoracic echocardiogram showed concentric left ventricular hypertrophy, normal global and regional contractile function, and minor valvular disease. Pending the analysis of BAL fluid, trimethoprim-sulfamethoxazole, levofloxacin, ceftriaxone, and caspofungin were started. BAL yielded a sanguineous fluid with 770 WBC/mm3 consisting of 81% monocytes and macrophages, some of which were multinucleated. An iron stain showed that about 70% of the macrophages were iron-loaded. Tests for Pneumocystis jiroveci (fluorescence microscopy), Legionella, Mycoplasmapneumoniae, respiratory syncytial virus, and Mycobacterium tuberculosis complex were all negative. The patient progressed to respiratory failure requiring mechanical ventilation. A thoracoscopic lung biopsy was performed. Light microscopy showed intraalveolar bleeding and the presence of hemosiderin-loaded macrophages, without vasculitis, necrosis, or extensive inflammation (Figs 1, 2), consistent with a diagnosis of diffuse alveolar hemorrhage. A tentative diagnosis of everolimus-associated diffuse alveolar hemorrhage was made. Everolimus was discontinued, the antimicrobial agents were withdrawn, and corticosteroids (methylprednisolone 64 mg daily) were initiated. This resulted in rapid improvement of the respiratory status, enabling the patient to be weaned off the ventilator within 5 days. Methylprednisolone was tapered over the following weeks to a maintenance dosage of 4 mg daily.