In normal subjects the gastrointestinal tract is a relatively impermeable barrier to
aluminum with a low fractional absorption rate for this
metal ion.
Aluminum absorbed from the gastrointestinal tract is normally excreted by the kidneys; in the presence of impaired renal function
aluminum is retained and accumulates in body tissues.
Aluminum-containing medications are given, by mouth, to patients with
chronic renal failure as
phosphate-binding agents for the therapeutic control of
hyperphosphatemia. Patients with
chronic renal failure are also exposed to
aluminum in domestic tap-water supplies used either for drinking or, in those on dialysis treatment, in the preparation of their
dialysate. In patients with end-stage
chronic renal failure, particularly in those on treatment by
hemodialysis, the accumulation of
aluminum in bone, brain, and other tissues is associated with toxic sequelae. An increased brain content of
aluminum appears to be the major etiological factor in the development of a neurological syndrome called either "dialysis
encephalopathy" or "dialysis
dementia"; an increased bone content causes a specific form of
osteomalacia. An excess of
aluminum also appears to be an etiological factor in a microcytic,
hypochromic anemia that occurs in some patients with
chronic renal failure on long-term treatment with
hemodialysis. The various mechanisms involved in the toxic phenomena associated with the accumulation of
aluminum in body tissues have not been clearly defined but are the subject of extensive investigations.