Accumulation of Aluminium in Patients with Acute Renal Failure

Abstract

Serum aluminium was monitored in 19 patients admitted with acute oligo-anuric renal failure. The maximum serum aluminium obtained during the course of treatment was greater (p < 0.05) in 4 patients treated by haemodialysis alone, mean ± sem 3.78 ± 0.71 μmol/l than in 4 patients treated only by haemofiltration, 0.60 ± 0.22 μmol/l. For those 11 patients treated by both haemodialysis and haemofiltration, the maximum serum aluminium was greater (p < 0.05) during treatment with haemodialysis, 2.7 ± 0.62 μmol/l than during treatment with haemofiltration, 1.36 ± 0.15 μmol/l. There was a significant positive correlation between the maximum serum aluminium during treatment with haemodialysis and the number of hours of haemodialysis given (r = 0.76, p < 0.001). There was no significant increase in serum aluminium due to the administration of human albumin solutions. The aluminium content of dialysate water represents a major source of aluminium in patients with acute renal failure; prevention by reverse-osmosis water purification is recommended.

Different Mg to Fe Ratios in the Mixed Metal MgFe Hydroxy-Carbonate Compounds and the Effect on Phosphate Binding Compared With Established Phosphate Binders

“…However, the most commonly used binders are not only relatively ineffective but also contain aluminum or calcium. Aluminum can cause neurological, skeletal, and hematological toxicity,14–21 whereas calcium leads to hypercalcemia and soft tissue calcification 22–26. The alternative phosphate binder, Mg(OH) 2 , is effective, but is poorly tolerated and associated with high ionic Mg release, resulting in diarrhea and hypermagnesemia 27–33.…”

The development and in-vitro evaluation of novel mixed metal hydroxy-carbonate compounds as phosphate binders

“…However, evidence shows that the aluminium absorbed from the gastrointestinal tract after dosing with such compounds is not removed by dialysis (Powell & Thompson 1993). Thus, haemodialysis patients are prone to accumulate aluminium (Davenport & Roberts 1989 ;Salusky et al 1991), which may cause dialysis encephalopathy and other long-term haematological and neurological problems (Alfrey et al 1976). The current binders of choice are calcium-containing salts, such as calcium carbonate and calcium acetate, which have been used with varying degrees of success (Llach & Bover 1996).…”

The evaluation of novel mixed metal hydroxy-carbonates as phosphate binders: an in-vivo study in the rat

“…Dietary phos-phate burden is therefore controlled by ingestion of binders, reducing availability for absorption. The current therapies of choice, CaCO 3 and Al(OH) 3 , are however associated with hypercalcaemia and aluminium accumulation\toxicity, respectively (Coburn & Salusky 1989 ;Davenport & Roberts 1989 ;Sherrard 1991). In addition, CaCO 3 is an inefficient binder and has to be used in large doses of up to 20 g per day (Schaefer et al 1988).…”

“…However, studies show that aluminium in these compounds is absorbed from the gastrointestinal tract and is not removed by dialysis (Powell & Thompson 1993). Thus, haemodialysis patients are likely to accumulate significant amounts of aluminium (Davenport & Roberts 1989). This accumulation of aluminium may cause dialysis encephalopathy, microcytic anaemia and osteomalacia (Alfrey et al 1976 ;Parkinson et al 1979 ;Short et al 1980).…”