DIALYSATE CALCIUM REDUCTION IN CAPD PATIENTS TREATED WITH CALCIUM-CARBONATE AND ALFACALCIDOL

The use of oral calcium carbonate as a phosphate binder is often compl icated by hypercalcaemia, particularly with concomitant use of vitamin D analogues. We previously found that stepwise reduction of dialysate calcium effectively countered this complication in haemodialysis pati ents, and have now assessed the strategy in CAPD patients. Seventeen p atients underwent conversion from aluminium hydroxide to calcium carbo nate and were followed for 5 months, with subsequent addition of alfac alcidol for a further 5 months. Standard CAPD dialysate (1.75 mM calci um) was used, reducing to 1.45 mM and, if necessary, to 1.00 mM in pat ients who became hypercalcaemic. While receiving calcium carbonate alo ne, 12 of the 17 patients became hypercalcaemic, this responding in fo ur to dialysate calcium reduction to 1.45 mM. In the remaining eight p atients, further reduction to 1.00 mM was required and in two patients even this failed to control hypercalcaemia adequately, necessitating reversion to aluminium hydroxide. Phosphate control remained unchanged , as did calcium x phosphorus product. There were transient increases of blood ionised calcium, and decreases of parathyroid hormone, with p rogressive reduction of serum aluminium and alkaline phosphatase. The addition of alfacalcidol (0.25-mu-g/day) led to hypercalcaemia in six subjects, successfully countered by dialysate calcium reduction in fou r. The results show that standard CAPD dialysate calcium at 1.75 mM is too high for the majority of calcium carbonate treated patients and t hat substantial reductions of the dialystate calcium concentration are required if calcium carbonate is to be used effectively.