The Use of Calcium Carbonate to Treat the Hyperphosphataemia of Chronic Renal Failure

This study evaluates the use of calcium carbonate in chronicrenal failure. Forty-eight patients (25 male, 23 female, meanage 54.3 years, six pre-dialysis, 12 CAPD, 30 haemodialysis)on phosphate restriction and requiring aluminium hydroxide (mean2.4±0.8 g/ day) to control serum phosphate, were convertedto an equivalent dose of calcium carbonate (2.5±0.6 g/day).None received vitamin D analogues. Three months post-conversionthere was a significant decrease in mean (±SEM) serumphosphate (1.86±0.08 versus 1.66±0.05 mmol/l,P<0.01) and serum aluminium (28.3±5.4 versus 13.2±3.0µg/l,P<0.0001); calcium/phosphate product was unchanged. Post-conversionthere was an increase in serum bicarbonate, (20.6±0.5versus 22.1±0.6 mmol/l, P<0.01) and serum calcium(2.32±0.02 versus 2.45±0.03 mmol/l, P<0.0001).No change in serum creatinine, alkaline phosphatase or parathormoneoccurred. No adverse effects were reported but nine (18%) patientsbecame hypercalcaemic (2.7 to 2.93 mmol/l), eight of whom respondedto dose reduction. Hypercalcaemia did not correlate with pre-conversionserum calcium, parathyroid hormone, alkaline phosphatase oraluminium. Calcium carbonate is an effective alternative toaluminium-based phosphate binders. It produces a beneficialincrease in serum calcium and bicarbonate and a significantdecrease in serum aluminium. Hypercalcaemia is unpredictablebut is easily reversible in the majority of patients.