LONG-TERM EFFECTS OF INTRAVENOUS 1-ALPHA(OH)D-3 COMBINED WITH CACO3 AND LOW-CALCIUM DIALYSIS ON SECONDARY HYPERPARATHYROIDISM AND BIOCHEMICAL BONE MARKERS IN PATIENTS ON CHRONIC-HEMODIALYSIS

The effects of intravenous administration of 1 alpha-hydroxycholecalci ferol [1 alpha(OH)D-3] in combination with CaCO3 and 'low-calcium dial ysis' (1.25 mmol/l) on plasma (p) parathyroid hormone (PTH) and bioche mical bone markers (osteocalcin, alkaline phosphatase, procollagen typ e 1 c-terminal extension peptide) were examined in 54 patients on chro nic hemodialysis with either normal or elevated PTH. Increasing doses of 1 alpha(OH)D-3 were administered intravenously under careful contro l of p-Ca2+ and inorganic phosphate. Blood samples were obtained 1 wee k before the start of treatment and then every 2nd week. 20 patients w ith initially normal PTH levels (23.5 +/- 4.17 pg/ml) and 34 patients with initially elevated PTH levels (301 +/- 45 pg/ml) were followed fo r up to 88 weeks. The present investigation demonstrated: (1) 'Low-cal cium hemodialysis' (1.25 mmol/l) made it possible to use larger doses of CaCO3 and to reduce the doses of an aluminium-containing oral phosp hate binder. A decrease in p-Ca2+ during dialysis was induced, and spe cial care had to focus on the compliance to CaCO3, in order not to agg ravate the secondary hyperparathyroidism. (2) The combination of 'low- calcium hemodialysis', CaCo3, and pulse intravenous 1 alpha(OH)D-3 pre vented the development of secondary hyperparathyroidism in patients wi th normal PTH levels and induced a long-term suppression of p-PTH (106 +/- 25 pg/ml, 88 weeks) in the patients with secondary hyperparathyro idism. By careful monitoring, severe hypercalcemia and hyperphosphatem ia were avoided. There were no indications, clinically or biochemicall y, of development of adynamic bone disease. (3) Bone lesions were heal ed and a decrease of the bone mineral content in lumbar spine and femo ral neck of patients with both normal and elevated PTH levels prevente d. (4) The present results may suggest that PTH might be of influence on the regulation of procollagen type 1 c-terminal extension peptide.