In dialysis centers using reverse osmosis-treated water but not restricting Al(OH)₃ administration, a high prevalence of histological aluminum bone disease has been reported. To assess wether this is also the case in our center where Al(OH)₃ intake has always been restricted and even completely given up after 1980 thanks to high doses of CaCO₃, we reviewed 42 bone biopsies performed between 1975 and 1985 in patients dialyzed for a mean duration of 56 months. Seventeen of these patients had been dialyzed before 1978 with softened water moderately contamined by aluminum, 15 had always been dialyzed with reverse osmosis-treated water and 10 had been exclusively treated by hemofiltration. The prevalence of aluminum bone disease in the whole population was 9.5% (4 patients) and consisted only of adynamic bone disease, osteomalacia being totally absent. When the patients dialyzed with aluminum-contaminated water were excluded as well as 1 diabetic patient who had taken Al(OH)₃ for 1.5 years the prevalence of aluminum bone disease was null in this population. When the whole population is considered the prevalence of the other types of bone disease was 76% for osteitis fibrosa and 14.5% for a non-aluminic adynamic bone disease (6 cases). These latter cases differed from the osteitis fibrosa group only by a relative hypoparathyroidism not explained by higher plasma concentrations and higher oral cumulative doses of calcium, magnesium and aluminum or by lower plasma concentrations of phosphate and bicarbonate. None had previous parathyroidectomy, one had an unsuccessful transplantation and one was diabetic. Iron overload was excluded by negative Perls staining. Duration of dialysis was shorter for these patients than for those with osteitis fibrosa. Conclusions: (1) In the absence of parenteral aluminum contamination, exclusion of Al(OH)₃ allows to prevent completely aluminic bone disease. (2) A new uremic bone disease is described: the idiopathic adynamic bone disease associated with a relative hypoparathyroidism.

Linear calcifications of the abdominal aorta and of the iliac and femoral arteries were measured yearly for 3 years on X rays of 24 patients on chronic hemodialysis taking variable amounts of calcium carbonate and Al(OH)₃ but no pharmacological doses of vitamin D or lα-hydroxylated vitamin D derivatives. The speed of their extension appeared exponential and covariant with the male sex, age only for men and, independently of these two factors, with diastolic blood pressure and blood triglycerides. Plasma concentrations of calcium, phosphate and glucose were covariant with the extension of calcinosis only at a borderline level. The doses of calcium carbonate and the levels of plasma alkaline phosphatase were not at all covariant. Conclusions: (1) The effect of high doses of calcium carbonate is possibly harmful only when supraphysiological levels of plasma calcium are induced, whereas plasma phosphate is not adequately decreased. The doses of calcium carbonate per se have no deleterious effect (2). Since alkaline phosphatase is not covariant with the extension of calcinosis, the degree of hyperparathyroidism per se does not seem to play a causative role in vascular calcinosis (3). The main risk factors of vascular calcinosis are: age, the male sexe, diastolic blood pressure and blood triglycerides.

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