Long-term effects of intermittent oral alphacalcidol, calcium carbonate and low-calcium dialysis (1.25 mmol L−1) on secondary hyperparathyroidism in patients on continuous ambulatory peritoneal dialysis
Article first published online: 26 AUG 2008
Blackwell Science Ltd, 1997
Journal of Internal Medicine
Volume 244, Issue 2, pages 121–131, August 1998
How to Cite
Brandi, Nielsen, Bro, Daugaard and Olgaard (1998), Long-term effects of intermittent oral alphacalcidol, calcium carbonate and low-calcium dialysis (1.25 mmol L−1) on secondary hyperparathyroidism in patients on continuous ambulatory peritoneal dialysis . Journal of Internal Medicine, 244: 121–131. doi: 10.1046/j.1365-2796.1998.00323.x
- Issue published online: 26 AUG 2008
- Article first published online: 26 AUG 2008
- 1α-hydroxycholecalciferol oral;
- continuous ambulatory peritoneal dialysis;
- parathyroid hormone;
- secondary hyperparathyroidism
Brandi L, Nielsen PK, Bro S, Daugaard H, Olgaard K (Rigshospitalet, University of Copenhagen, Denmark). Long-term effects of intermittent oral alphacalcidol, calcium carbonate and low-calcium dialysis (1.25 mmol L−1) on secondary hyperparathyroidism in patients on continuous ambulatory peritoneal dialysis. J Intern Med 1998; 244: 121–31.
(i) To examine the effect of alphacalcidol [1α(OH)D3] given as an oral dose twice weekly in combination with CaCO3 and low-calcium dialysis (1.25 mmol L−1) on the secondary hyperparathyroidism in continuous ambulatory peritoneal dialysis (CAPD). (ii) To examine the changes in peritoneal mass transfer for calcium, phosphorus, magnesium, lactate, creatinine, urea, glucose, pH and albumin after shift to low-calcium dialysis solution.
An open study in patients on CAPD.
Renal division, Rigshospitalet, Copenhagen.
Thirty-nine patients were included and completed 12 weeks of treatment. Thirty of the patients completed 52 weeks of treatment. A peritoneal equilibrium test (PET) was performed in seven patients.
Following two sets of blood samples obtained as basal values the calcium concentration was reduced in the dialysis fluid from 1.75 mmol L−1 to 1.25 mmol L−1. Increasing doses of oral 1α(OH)D3 were then administered under careful control of p-ionized calcium (p-Ca2+) and p-inorganic phosphate (p-Pi). Blood samples were obtained every 2–4 weeks for 52 weeks. PET was performed using standard dialysis fluid and 1 week later using low-calcium dialysis fluid after a preceding overnight dwell. Two litres of glucose 22.7 mg mL−1 were used.
Main outcome measures
Intact parathyroid hormone (PTH), p-Ca2+, p-Pi, doses of CaCO3, doses of 1α(OH)D3, peritoneal mass transfer for calcium, inorganic phosphate, magnesium, lactate, creatinine, urea, glucose and albumin.
Thirty nine patients with initial PTH values 144 ± 26 pg mL−1 were followed for 12 weeks and 30 patients for 52 weeks. A negative calcium balance was induced after shifting to low-calcium dialysis fluid. After 2 weeks of treatment a significant increase of PTH by approximately 60% and a small but significant decrease of p-Ca2+ was observed. After 12 weeks of treatment with increasing doses of 1α(OH)D3 and CaCO3, PTH was again reduced to levels not significantly different from the initial values. After 52 weeks of treatment no deterioration of the secondary hyperparathyroidism was seen.
A calcium concentration of 1.25 mmol L−1 in the CAPD dialysate made it possible to reduce the amount of aluminium-containing phosphate binder, to increase the doses of CaCO3 and to use pulse oral 1α(OH)D3 without causing severe hypercalcaemia in the patients. After a short elevation of PTH, the PTH levels remained at normal or near normal levels and the long-term results clearly demonstrated that an aggravation of the secondary hyperparathyroidism could be inhibited.