Abstract
In the first study, 46 hemodialysis patients were divided into two groups: patients in the “AI” group continuously took AI (OH)3 with 1α(OH)D3 daily for 6 months, and patients in the “Ca” group were withdrawn from any aluminum compounds and took CaCO3 with lα(OH)D3 for 6 months. Serum AI levels markedly decreased from 69.2±34.3μg/l to 37.7±36.1μg/l (p<0.01) in the “Ca” group, while there was only a slight decrement in the “AI” group. ΔAI by DFO test also decreasted significantly from 141±93μg/l to 77.4±63.1μg/l (p<0.01). These results indicate that AI accumulation in uremics is caused not only by the AI-contaminated dialysate but also by oral ingestion of AI compounds. In the second study, we developed a new method of CaCO3 administration in order to prevent hypercalcemia of patients with renal osteodystrophy, namely, the alternative administration of CaCO3/1α(OH)D3. In this method, 1α(OH)D3 was given only three times a week (the days of hemodialysis) and CaCO3 was given only during the rest of the week. Eight of 13 patients who could not take 1α(OH)D3 because of hypercalcemia were successfully treated by both drugs without hypercalcemia by this method. The patients who failed this mode of therapy were considered to have osteomalacia.
