Long-Term Effects of Intravenous 1α(OH)D3 Combined with CaCO3 and Low-Calcium Dialysis on Secondary Hyperparathyroidism and Biochemical Bone Markers in Patients on Chronic Hemodialysis

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Abstract
The effects of intravenous administration of 1 α-hydroxycholecalciferol [lα(OH)D3] in combination with CaCO3 and ‘low-calcium dialysis’ (1.25 mmol/l) on plasma (p) parathyroid hormone (PTH) and biochemical bone markers (osteocalcin, alkaline phosphatase, procollagen type 1 c-terminal extension peptide) were examined in 54 patients on chronic hemodialysis with either normal or elevated PTH. Increasing doses of lα(OH)D3 were administered intravenously under careful control of p-Ca2+ and inorganic phosphate. Blood samples were obtained 1 week before the start of treatment and then every 2nd week. 20 patients with initially normal PTH levels (23.5 ± 4.17 pg/ml) and 34 patients with initially elevated PTH levels (301 ± 45 pg/ml) were followed for up to 88 weeks. The present investigation demonstrated: (1) ‘Low-calcium hemodialysis’ (1.25 mmol/l) made it possible to use larger doses of CaCCO3 and to reduce the doses of an aluminium-containing oral phosphate binder. A decrease in p-Ca2+ during dialysis was induced, and special care had to focus on the compliance to CaCCO3, in order not to aggravate the secondary hyperparathyroidism. (2) The combination of ‘low-calcium hemodialysis’, CaCCO3 and pulse intravenous lα(OH)D3 prevented the development of secondary hyperparathyroidism in patients with normal PTH levels and induced a long-term suppression of p-PTH (106 ± 25 pg/ml, 88 weeks) in the patients with secondary hyperparathyroidism. By careful monitoring, severe hypercalcemia and hyperphosphatemia were avoided. There were no indications, clinically or biochemically, of development of adynamic bone disease. (3) Bone lesions were healed and a decrease of the bone mineral content in lumbar spine and femoral neck of patients with both normal and elevated PTH levels prevented. (4) The present results may suggest that PTH might be of influence on the regulation of procollagen type 1 c-terminal extension peptide.

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