Abstract: SA-PO1204
Neurological Manifestations in a Kidney Transplant Recipient: An Unexpected Case of Manganese (Mn) Toxicity
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
- Vaishnav, Sakshi, Medical University of South Carolina, Charleston, South Carolina, United States
- Edding, Sherida, Medical University of South Carolina, Charleston, South Carolina, United States
- Posadas, Maria Aurora C., Medical University of South Carolina, Charleston, South Carolina, United States
- McMahon, Blaithin A., Medical University of South Carolina, Charleston, South Carolina, United States
Introduction
Mn toxicity is a rare disorder causing neuropsychiatric symptoms. It has been reported in miners, patients on hemodialysis, on prolonged parenteral nutrition, and chronic liver disease with portosystemic shunting. However, Mn toxicity after kidney transplantation (KT) with a functioning allograft has not been previously reported.
Case Description
We describe a 46/F with Budd-Chiari syndrome (BCS) s/p TIPS and ESRD from congenital obstructive uropathy, s/p DDKT (2021), presenting with one month of tremors, gait instability, intermittent aphasia, and altered awareness. Brain MRI showed T1 hyperintensity of the globus pallidus (GP), the differential for which includes Mn toxicity. Serum Mn was elevated at 14.9 µg/L (ref: 0.5–1.2 µg/L), with stable graft function.
Chelation with calcium disodium EDTA was initiated but stopped early due to AKI. Despite this, she had biochemical improvement and partial clinical recovery. Allograft biopsy showed severe chronic changes without rejection.
Discussion
Mn is an essential trace element cleared via hepatobiliary excretion with minimal renal elimination. Neurotoxicity results from GP deposition. Diagnosis relies on history, symptoms, imaging, and Mn levels. Hemodialysis is ineffective at clearing Mn due to high protein binding, while EDTA increases urinary excretion but is nephrotoxic and less effective after CNS deposition.
BCS with TIPS likely impaired hepatic metabolism, leading to Mn accumulation. Mn toxicity should be considered in transplant recipients with unexplained neurologic symptoms, especially those with portosystemic shunting. Early recognition is critical, as deficits may persist despite normalization of levels.