• J G Heaf, J Pødenphant, P Joffe, J R Andersen, S Fugleberg, and O Braendstrup.
• Department of Nephrology, Hvidovre Hospital.
• Scand J Urol Nephrol. 1987 Jan 1; 21 (3): 229-33.

Abstract12 patients with conservatively treated uremia were investigated using bone histomorphometry, bone aluminium concentration determination and total body bone mineral content (TBBM). The bone aluminum was raised in 10 patients and was significantly related to oral aluminium salt consumption (p less than 0.01). Two of four patients who had not received aluminium also had raised levels but the difference was not significant from nonuremic patients. The two patients with the highest levels had a mineralisation defect despite normal levels of 1,25-dihydroxyvitamin D. Three patients had significant bone loss of whom one had osteomalacia (OM) while two had secondary hyperparathyroidism (2HP). It is concluded that 1) aluminium salt consumption results in bone aluminium accumulation, and may contribute to the mineralisation defect; 2) uremic patients not treated ith aluminium salts may have slightly raised levels, but this seems not to be clinically important; 3) secondary hyperparathyroidism causes greater destruction of bone mass than other uremic bone diseases; 4) atomic absorption spectrometry is a more sensitive method for detecting aluminium bone deposition than histochemical methods.

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