Abstract Hydralazine is a recognized trigger of drug-induced lupus and, less commonly, antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. Diffuse alveolar hemorrhage (DAH) is a rare life-threatening pulmonary manifestation. We report a case of DAH in a kidney-transplant recipient receiving chronic hydralazine therapy. An 86-year-old African American man with type 2 diabetes, hypertension, chronic atrial fibrillation, and end-stage renal disease status post deceased-donor kidney transplant (2023) with chronic allograft dysfunction (CKD5) presented with two weeks of dyspnea, orthopnea, and bilateral edema to an outside hospital. Home medications included hydralazine 50 mg three times daily. He presented to our institution in septic shock requiring vasopressors and intubation. Urine culture grew Klebsiella pneumoniae; meropenem, vancomycin, and azithromycin were administered. Chest CT showed bilateral diffuse/alveolar opacities. Bronchoscopy with bronchoalveolar lavage completed on day 1 demonstrated DAH with increasingly bloody serial aliquots. Repeat bronchoscopy on day 3 revealed no evidence of ongoing hemorrhage. A comprehensive respiratory infectious evaluation including cultures, viral and fungal testing, pneumocystis, legionella, parasitic workup was unrevealing. Transplant virology showed low plasma EBV viremia and low BK viremia. Autoimmune testing supported a hydralazine-triggered process: ANA 1:640 (cytoplasmic pattern), RNP antibody positive, threshold positive anti-histone, complements within range, and negative dsDNA, ANCA, anti-GBM, Scl-70, centromere, and rheumatoid factor. Hydralazine was discontinued. High dose corticosteroids and nebulized tranexamic acid were administered. Anticoagulation was resumed on day 5. He remained intubated for 8 days. Continuous renal replacement therapy (RRT) was required during his critically ill phase without need for ongoing dialysis. Hydralazine-triggered autoimmune reactions manifesting as DAH is rare; More commonly, hydralazine related pulmonary complications are through an ANCA-associated vasculitis phenotype, whereas this patient’s serology favored drug-induced lupus (high-titer ANA with cytoplasmic staining, RNP positivity, borderline anti-histone, normal complements, and negative MPO/PR3-ANCA, dsDNA, and anti-GBM). The solid-organ transplant setting further heightens complexity: chronic tacrolimus, CKD5 allograft dysfunction, and low-level EBV and BK viremia widen the differential to infectious and inflammatory etiologies due to immunosuppression. The case required carefully sequenced trade-offs: immediate hydralazine withdrawal; high dose corticosteroids in a septic and immunosuppressed host; nebulized tranexamic acid for local hemostasis, RRT and time-sensitive resumption of apixaban for atrial fibrillation after resolution of hemorrhage. Successful liberation from ventilation, and renal recovery—supports a diagnosis of hydralazine-triggered DAH. Awareness of hydralazine as a trigger of DAH—distinct from ANCA-associated vasculitis—is critical, especially in immunocompromised hosts where sepsis and cardiogenic edema may confound diagnosis. Immediate discontinuation and immunosuppression remain cornerstone therapy. This abstract is funded by: None
Rodriguez et al. (Fri,) studied this question.