Aluminium load in patients with analgesic nephropathy

It is well-known that plasma aluminium in haemodialysis patients increases with the amount of aluminium hydroxide consumption. In a cross-sectional study at our haemodialysis centre we found that mean plasma aluminium levels are significantly higher in haemodialysis patients with analgesic-associated nephropathy (AAN) than in haemodialysis patients with other kidney diseases (controls) (logarithmic mean +/- SD = 1.93 +/- antilog 0.32 versus 1.21 +/- antilog 0.31 mumol/l; p = 0.001). AAN patients consume a significantly higher amount of aluminium-containing phosphate binders than the controls (21 +/- antilog 0.3 versus 13 +/- antilog 0.4 g/kg body weight/year; p = 0.007). These findings may be explained by the higher incidence of peptic ulcer disease in AAN patients, since hyperacidity decreases the phosphate-binding effect. Analgesic patients also need more aluminium-containing stomach medication than do patients with other kidney diseases (0.21 +/- antilog 1.15 versus 0.03 +/- antilog 0.87 g/kg body weight/year; p = 0.0001). A statistically significant correlation was obtained between bone aluminium and duration of phosphate binder consumption (r = 0.6459; n = 14; p less than 0.05). There was no correlation between plasma aluminium and bone aluminium. Anaemia was more pronounced in the AAN patients than in the others (mean haemoglobin 8.4 +/- 1.9 vs. 9.2 +/- 2.0 g%; p less than 0.02). Dialysis dementia was observed in 4 AAN patients. We conclude that the higher plasma aluminium levels in AAN patients represent a higher aluminium load which may be followed by higher aluminium toxicity.