What does this research mean for the field?

Manganese toxicity can occur in functioning kidney transplant recipients, presenting with severe neurological symptoms and MRI abnormalities that partially respond to chelation therapy despite the risk of renal function decline. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To describe a case of manganese toxicity in a kidney transplant recipient and highlight associated neurological symptoms.

May 19, 2026Cureus0 citationsOpen Access

Neurological Manifestations in a Kidney Transplant Recipient: An Unexpected Case of Manganese Toxicity

SVSakshi VaishnavMedical University of South Carolina SESherida EddingMedical University of South Carolina APAurora PosadasMedical University of South Carolina

Key Points

To describe a case of manganese toxicity in a kidney transplant recipient and highlight associated neurological symptoms.
Patient underwent kidney transplantation in 2021.
Brain MRI and serum manganese levels were assessed.
Chelation therapy was initiated but discontinued due to renal function decline.
Patient had elevated serum manganese at 14.9 µg/L (reference range 0.5-1.2 µg/L).
Brain MRI showed T1 hyperintensity in the globus pallidus, indicating manganese deposition.
Partial clinical recovery occurred despite early cessation of chelation therapy.

Abstract

Manganese (Mn) toxicity is a relatively uncommon neurotoxic condition characterized by neuropsychiatric symptoms and parkinsonism. We describe a 46-year-old woman with end-stage renal disease due to congenital obstructive uropathy, status post deceased-donor kidney transplantation (2021), who presented with one month of worsening tremors, gait instability, intermittent aphasia, and altered awareness. Brain magnetic resonance imaging demonstrated persistent but improved T1 hyperintensity of the globus pallidus compared to prior imaging, consistent with Mn deposition. Serum Mn was markedly elevated at 14.9 µg/L (reference range 0.5-1.2 µg/L). Chelation therapy with calcium disodium ethylenediaminetetraacetic acid was initiated but discontinued early due to decline in renal function. Despite early cessation, treatment resulted in biochemical improvement and partial clinical recovery. Kidney allograft biopsy, performed due to a rise in creatinine during the hospital course, demonstrated severe chronic changes without evidence of acute rejection. Thorough history taking and evaluation of environmental factors did not identify a clear source of Mn exposure. The patient's history was notable for Budd-Chiari syndrome with portal hypertension status post transjugular intrahepatic portosystemic shunt, which likely contributed to impaired Mn clearance. To our knowledge, Mn toxicity occurring in a functioning kidney transplant recipient has not previously been reported. This case underscores the diagnostic and therapeutic challenges of Mn toxicity.

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