Abstract
Deferoxamine is widely used in the diagnosis and treatment of aluminum toxicity and has a characteristic combination of side effects, including a poorly defined worsening of existing neurologic symptoms. However, to date, no measurement of cerebrospinal fluid (CSF) aluminum concentrations after deferoxamine exist. We report the case of a patient who developed acute neurological deterioration in conjunction with sepsis and elevated serum aluminum levels shortly after renal transplantation. Simultaneous values for blood and CSF aluminum were measured in response to deferoxamine and hemodialysis. The increase in CSF aluminum levels appears to parallel that seen in serum after deferoxamine. We hypothesize that this elevation in CSF aluminum may account for the observed neurologic deterioration after deferoxamine and postulate various pathophysiologic mechanisms that might be involved.
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