Elevated concentration of aluminum has been reported in serum, whole blood and tissue samples of patients with renal insufficiency. Evidence incriminating aluminum as a neurotoxin among the dialysis population is strong. The source of this aluminum has not been clearly defined, although both gastrointestinal and parenteral routes may be involved. Data from this laboratory suggest that an effect of parathyroid hormone on tissue aluminum burdens may, in part, explain why only certain patients exposed to high dialysate aluminum develop the dialysis encephalopathy syndrome and the occasional occurrence of this syndrome in the absence of dialysis or increased dialysate aluminum.