Aluminium is a non-essential trace element of ubiquitous distribution. Although exposure to aluminium dust in industrial situations has been associated with pulmonary fibrosis, most cases of aluminium toxicity have been in patients with chronic renal failure (CRF) on haemo- or peritoneal dialysis. Greatly elevated plasma aluminium concentrations in these patients are clearly associated with the symptoms of dialysis encephalopathy and osteodystrophy. Aluminium accumulation may be possible, in part at least, for the anaemia and soft tissue calcification of CRF. The increased body burden arises from two sources. Firstly, oral aluminium hydroxide was widely used as a phosphate binder and secondly aluminium is added to reservoir water as a flocculent. In recent years magnesium salts have replaced aluminium hydroxide as an intestinal phosphate binder and most dialysis units now have reverse osmosis units to purify water for dialysis prior to use. High plasma aluminium concentrations are less common in CRF patients now but continued monitoring is required.
Aluminium is transported in blood bound to transferrin, and aluminium status is best assessed by measurement of the plasma aluminium concentration. In addition, the aluminium content of the dialysis solutions and water used for dilution may also require measurement.