High-normal calcium (1.35 mmol/l) dialysate in patients on CAPD: efficient and safe long-term control of plasma calcium, phosphate, and parathyroid hormone.Nephrol Dial Transplant. 1996 Aug; 11(8):1586-91.ND
The aim of the present study was to examine the long-term efficacy and safety of treatment with a high-normal calcium dialysate with a calcium concentration of 1.35 mmol/l in patients on CAPD. This dialysate calcium concentration is close to the high-normal plasma ionized calcium level aimed at in dialysis patients in order to suppress the parathyroid hormone secretion. The end-points of the study were (1) plasma ionized calcium (iCa) and phosphate (P) levels, (2) plasma intact parathyroid hormone (PTH) levels, (3) doses of calcium carbonate and alfacalcidol, (4) requirements of Al-containing phosphate binders, and (5) bone mineral density (BMD).
Thirty-seven non-selected patients on CAPD treatment were followed for an average of 10 months after switching from a dialysate Ca of 1.75 to 1.35 mmol/l. After 1 week, a significant decrease of mean iCa from 1.26 +/- 0.01 to 1.23 +/- 0.01 mmol/l (P < 0.05) and an increase of median PTH from 80 to 135 pg/ml (P < 0.01) were seen. From the 2nd week and onwards, however, basal levels of iCa and PTH were restored and remained stable. mean plasma iCa was kept within 1.23-1.31 mmol/l; mean plasma P below 1.65 mmol/l and median PTH within 52-135 pg/ml. Episodes of hypercalcaemia were few (1.2 cases of plasma iCa > 1.45 mmol/l per 100 treatment weeks), and the need for Al-containing P binders low with only five patients requring this treatment for isolated and four patients for repeated episodes of hyperphosphataemia or hypercalcaemia. After switching from a dialysate Ca of 1.75 to 1.35 mmol/l, the doses of calcium carbonate and alfacalcidol could be significantly increased. Furthermore, using the dialysate Ca of 1.35 mmol/l made it possible to induce a controlled increase of PTH levels to 80-100 pg/ml by a temporarily discontinuation of alfacalcidol and/or a reduction of calcium carbonate dosage in the patients where PTH had become suppressed to levels below the upper normal limit. The intention of the treatment was to maintain PTH levels within 1.5-2.5 times the upper normal limit for non-uraemic patients. Pre-study BMD of the vertebral bodies L2-L4 and of the femoral neck were normal and not significantly different from post-study measurements.
The present study demonstrated that when using a high-normal dialysate Ca concentration of 1.35 mmol/l in non-selected patients on CAPD treatment, high-normal plasma iCa and near-normal plasma P levels could be readily achieved with a minimal risk of incidental hypercalcaemia despite use of calcium carbonate as the main P binder. As a consequence of the tight Ca and P regulation, minimal doses of alfacalcidol were required to keep PTH within acceptable limits. We recommend this dialysate Ca concentration as a first-choice therapy for the majority of patients starting on CAPD treatment.