A randomized trial comparing 1.25 mmol/l calcium dialysate to 1.75 mmol/l calcium dialysate in CAPD patients

Effective control of hyperparathyroidism and renal osteodystrophy in CAPD patients requires a combination of calcitriol and calcium carbonate (CaCO3), but is frequently limited by hypercalcaemia. Reducing dialysate calcium (Ca) concentration may overcome this problem, but had not been examined in a controlled trial.

45 stable CAPD patients were randomly assigned in a prospective double-blind trial to either a study group (1.25 mmol/l Ca dialysate) or a control group (1.75 mmol/l Ca dialysate) for 12 months. Clinical, biochemical and radiological parameters of secondary hyperparathyroidism were followed.

Twenty-three patients did not complete the study due to death (9), transplantation (7) or conversion to haemodialysis (7). Eleven patients in each group completed the study. Mean serum Ca, phosphate, ionized Ca, aluminium, alkaline phosphatase (AP), and bone mineral density (BMD) Z-scores did not differ significantly at any time within or between the two groups. Severe hypercalcaemia was more common in the control group (11 vs. 2, P = 0.027). Mean serum intact parathyroid hormone (PTH) and osteocalcin (OCN) initially rose in the study group relative to controls at 3 months (40 +/- 7 vs 12 +/- 3 pmol/l, P = 0.004, and 33 +/- 5 vs 15 +/- 2 micrograms/l, P = 0.002 respectively), but were not sustained. Median weekly dosages of calcitriol and daily dosages of CaCO3 increased significantly in the study group (O microgram to 1 microgram P = 0.014 and 1260 mg to 2520 mg P = 0.002 respectively), but not in the control group. Supplementary aluminium hydroxide (A1, (OH)3) was required for phosphate control in both study (n = 5) and control patients (n = 4).

Lowering dialysate calcium concentration reduced the frequency of severe hypercalcaemia and allowed prescription of larger quantities of calcitriol and CaCO3. However, in this study it offered no advantage in terms of A1(OH)3 requirement, while bone mass density did and may have initially exacerbated secondary hyperparathyroidism not change.