Antiglomerular basement membrane (anti-GBM) disease causes rapidly progressive glomerulonephritis and diffuse alveolar hemorrhage (DAH) through autoantibodies directed against the α3 chain of type IV collagen. Evidence guiding adaptation of standard induction therapy (plasmapheresis, high-dose glucocorticoids, cyclophosphamide) for nonrenal solid organ transplant recipients remains scarce. A 55-year-old man, 9 years post-deceased donor liver transplantation for nonalcoholic steatohepatitis and maintained on low-dose tacrolimus, presented with pulmonary renal syndrome, severe metabolic acidosis, and high-titer anti-GBM antibodies. High-resolution computed tomography demonstrated bilateral ground-glass opacities consistent with DAH. He was treated with plasma exchange (seven sessions) and high-dose corticosteroids. Tacrolimus was discontinued, and maintenance immunosuppression was transitioned to mycophenolate mofetil with low-dose prednisone. Pulmonary hemorrhage resolved and anti-GBM titers declined to near the assay threshold; however, kidney function did not recover, and he remained dependent on hemodialysis. Four months later, he died of multidrug-resistant