Hypercalcaemia, hypermagnesaemia, hyperphosphataemia and hyperaluminaemia in CAPD: improvement in serum biochemistry by reduction in dialysate calcium and magnesium concentrations.

Phosphate binders are necessary to control hyperphosphataemia in the majority of dialysis patients. Whilst aluminium salts are efficient phosphate binders, their use is associated with toxic side effects. Calcium salts are a widely used alternative, but hypercalcaemia is a common side effect, limiting their use and raising concern about metastatic calcification. Reduction of the dialysis fluid calcium concentration has been shown to reduce hypercalcaemia in haemodialysis patients, with an associated decrease in serum PTH. We analysed the effect of reduced calcium/magnesium (1.25/0.25 mmol/l), 40 mmol/l lactate, PD fluid (PD4) on 11 CAPD patients with uncontrollable hypercalcaemia (> 2.65 mmol/l) and hyperphosphataemia (> 1.80 mmol/l). Only 1 patient remained hypercalcaemic, while phosphate fell in 6 patients (2.23 +/- 0.16 on no binder, to 1.68 +/- 0.08 mmol/l at 6 months (p < 0.05), but was unchanged in 5 (2.10 +/- 0.15 to 2.48 +/- 0.14 mmol/l [p = NS]). Overall mean calcium x phosphate product changed little. However, in a subgroup it fell significantly (p < 0.05). Geometric mean iPTH rose, but not significantly. The subgroup of patients whose calcium x phosphate product fell, exhibited a much smaller rise in iPTH than the others (57.3-73.2 vs. 52.8-167.1 pg/ml). 1.25-Dihydroxyvitamin D3 was subnormal in all patients. Mean serum magnesium fell from 1.24 +/- 0.06 to 0.89 +/- 0.04 mmol/l (p < 0.001), whilst mean serum bicarbonate rose significantly (25.2 +/- 0.4 to 28.9 +/- 1.2 mmol/l; p < 0.01). Withdrawal of aluminium-containing phosphate binders resulted in mean serum aluminium falling significantly from 31.1 +/- 5.7 at start of PD4 to 15.4 +/- 2.7 mu g/l at 6 months (p < 0.05). In summary, in around 50% of CAPD patients with persistent hypercalcaemia and hyperphosphataemia, reduction in PD fluid calcium can produce significant improvement in phosphate, reduction of calcium x phosphate product, and enable avoidance of aluminium-containing phosphate binders. Patients whose calcium and phosphate control remains poor, still benefit from the reduction, or cessation, of oral aluminium intake.