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.