Abstract: SA-PO1205
Autoimmune Glial Fibrillary Acidic Protein (GFAP) Astrocytopathy in a Kidney Transplant Recipient
Session Information
- Transplantation: Clinical - Complications, Pediatrics, and Multi-Organ Considerations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Sridhara, Srilekha, Mayo Foundation for Medical Education and Research, Phoenix, Arizona, United States
- Abu Jawdeh, Bassam G., Mayo Foundation for Medical Education and Research, Phoenix, Arizona, United States
- Alasfar, Sami, Mayo Foundation for Medical Education and Research, Phoenix, Arizona, United States
- Nair, Sumi, Mayo Foundation for Medical Education and Research, Phoenix, Arizona, United States
- Me, Hay Me, Mayo Foundation for Medical Education and Research, Phoenix, Arizona, United States
Introduction
Autoimmune encephalitis presents with neurological symptoms including altered mental status, seizures, memory deficits, and psychiatric manifestations such as psychosis. Evaluation requires exclusion of infectious, metabolic, toxic, vascular, and paraneoplastic causes. In renal transplant recipients, diagnosis and management are complex due to chronic immunosuppression.
Case Description
A 65-year-old female with end-stage kidney disease due to IgA nephropathy underwent living-related kidney transplantation 13 years prior. Her course was complicated by renal cell carcinoma requiring nephrectomy, COVID-19 infection, and recurrent urinary tract infections leading to reduced immunosuppression. Baseline creatinine was 2.2 mg/dL (eGFR 23 mL/min). Maintenance therapy included tacrolimus, mycophenolate, and prednisone.
She presented with altered mental status, memory and speech impairment, and hypersomnolence. Neuroimaging, cerebrospinal fluid studies, and PET-CT were non-contributory. GFAP antibody positivity (CBA titer 1:32) established the diagnosis of GFAP astrocytopathy.
Treatment included intravenous immunoglobulin and methylprednisolone followed by steroid taper. Mycophenolate was discontinued and tacrolimus transitioned to cyclosporine. Mental status improved; however, the course was complicated by recurrent pyelonephritis and varicella-zoster infection, leading to graft failure and initiation of renal replacement therapy. Cyclosporine was discontinued, and prednisone taper continued with gradual neurologic recovery.
Discussion
GFAP astrocytopathy involves antibodies against an astrocytic intracellular protein and may be associated with malignancy, supporting the role of PET-CT in evaluation. Management includes corticosteroids, IVIG, plasma exchange, and rituximab. In transplant recipients, treatment requires balancing immunosuppression with infection risk and graft function. This patient progressed to end-stage renal disease and is not a candidate for retransplantation.
Conclusion: GFAP astrocytopathy is a rare but important cause of encephalopathy in renal transplant recipients. Diagnosis requires high clinical suspicion and systematic evaluation. Management is challenging, requiring multidisciplinary coordination to balance immunologic treatment with infection risk and graft outcomes.