The predictive value of three different RIAs of PTH for the diagnosis of the histological type of bone disease has been compared in 24 asymptomatic patients on chronic hemodialysis who had never been exposed to aluminum intoxication and who agreed to have a bone biopsy after double tetracycline labeling. The serum concentrations of PTH were measured using a two-site immunoradiometric assay for intact PTH(1-84) and region specific assays directed against the C-terminal (53-84) fragment or the midregion (44-68) of the molecule. The bone histomorphometric analysis showed that six patients had nonaluminic adynamic bone disease with low bone formation rate (BFR), eight had mild hyperparathyroidism characterized by increased bone resorption and normal BFR, nine had severe hyperparathyroidism with increased BFR, and only one had true osteomalacia with increased osteoid seam thickness. All PTH assays correlated with the various parameters of bone resorption and bone formation and were able to differentiate the histological type of bone disease only when groups of patients were considered. For classifying individual patients into severe hyperparathyroidism and adynamic bone disease groups, the intact PTH assay had the best predictive value with a sensitivity of 100% and a specificity of at least 70%. A nonaluminic adynamic bone disease was observed in more than 50% of the patients who had normal intact PTH levels (6/11). It is concluded that the intact PTH measurement is superior to C-terminal and midregion assays for the prediction of the histological type of bone disease in hemodialyzed patients and should be of considerable value to adapt their treatment in order to avoid the emergence of both severe hyperparathyroidism and adynamic bone disease. In the absence of aluminum intoxication it seems that maintaining intact PTH concentrations 1 to 1.5 times the upper limit of normal would correspond to the best bone histology.

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.

To control hyperphosphataemia without hyperaluminaemia, A1(OH)3, which was given in addition to high doses of oral calcium, was replaced by Mg(OH)2 for 6 months in 20 haemodialysed patients and for 20 months in 12. The treatment during the control period was 110 +/- 91 mmol/day of oral calcium element given as CaCO3 and/or Calcium Sorbisterit and 1.05 +/- 1.47 g/day of A1(OH)3. Haemodialysis treatment was 4 h, thrice weekly. To prevent hypermagnesaemia, dialysate magnesium was decreased from 0.75 mmol/l to 0.375 mmol/l. After a control period of 3 months, Mg(OH)2 was given at a mean dose of 2.6 +/- 2 g/day and oral calcium supplements were decreased to 76 mmol/day. Two subsequent bone histomorphometry studies were performed at 8 month intervals in four patients and at 20 month intervals in seven patients. The results show a good control of plasma calcium (mean +/- SD: 2.43 +/- 0.1 mumol/l); phosphate (1.76 +/- 0.4 to 1.66 +/- 0.3 mmol/l); aluminum (1.3 +/- 0.1 mumol/l to 0.6 +/- 0.1 mumol/l); alkaline phosphatase (135 +/- 65 to 125 +/- 40 IU); and PTH fragments (PTH C terminal decreased from 260 +/- 214 to 185 +/- 182 pg/ml, PTH medium from 4185 +/- 5113 to 2270 +/- 4880 pg/ml). Plasma magnesium increased from 0.96 +/- 0.2 to 1.54 +/- 0.2 mmol/l. Bone histomorphometry shows no change in mineralisation, and a borderline decrease of resorption parameters. The main side-effects are (1) diarrhoea, which was well controlled by transient treatment with karaya gum, and (2) an increased need for potassium binders.(ABSTRACT TRUNCATED AT 250 WORDS)

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