Case Presentation: A 54 year old female with history of SLE, ESRD on hemodialysis, CAD and aortic valve replacement, was admitted for confusion that started the morning of admission. CT head, basic labs and urine toxicology were non-revealing. EEG recordings were consistent with subclinical non-convulsive status epilepticus and the patient was admitted to the ICU. Status persisted for several days despite treatment with Phenytoin and Levetiracetam. She underwent MRI brain, lumbar puncture and serologic testing to rule out lupus cerebritis or an infectious etiology, with no positive results. On closer review of home medications she was found to be on chronic sucralfate therapy which raised the possibility of aluminum toxicity. An aluminum level was ordered and the sucralfate discontinued. She was continued on anticonvulsants and hemodialysis with gradual dissipation of epileptiform discharges on EEG. She was then transferred to a long term acute care facility and continued on anti-epileptic drugs. Subsequently obtained results showed aluminum levels markedly elevated at 100mcg/L (Normal 0-9 mcg/L) and recommendations were made for deferoxamine stimulation and chelation therapy.

Discussion: Aluminum toxicity in end stage renal disease or dialysis dementia as it was once known has largely disappeared with the removal of aluminum from the water used for dialysis and the wide availability of nonaluminum-containing phosphate binders. Given the low prevalence of aluminum toxicity among dialysis patients, screening is now reserved for patients deemed to be at increased risk due to inadequate water purification systems, aluminum-based phosphate binder use or CKD related parathyroidism. Outbreaks at dialysis centers, few though they may be, have occurred and were linked to system or diasylate contamination. However there are other potential sources of aluminum we often overlook including medications frequently administered to dialysis patients such as calcitrol, clonidine, iron sulfate and calcium carbonate. The amount of these medications needed to cause toxicity is not known, but concurrent citrate use enhances intestinal aluminum absorption.

Conclusions: Dialysis dementia has been labeled “An Epidemic That Came and Went”, but is it really gone? Aluminum toxicity may now just be under-acknowledged in the ever-increasing population of dialysis patients and as such, perhaps we should review the indications for monitoring of aluminum levels. Although some factors are out of our control as physicians, careful medication reconciliation and awareness may save us from the diagnostic dilemma this entity once posed.