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 Acinetobacter pneumonia complicated by septic shock. To our knowledge, this represents the first reported case of de novo anti-GBM disease following liver transplantation. De novo Goodpasture syndrome can occur despite chronic immunosuppression in liver transplant recipients. Prompt recognition, individualized immunomodulation, and meticulous infection risk management are critical to controlling autoimmunity while preserving liver allograft function.
Solanki et al. (Mon,) studied this question.