The efficacy of
calcium carbonate (CaCO3) as a
phosphate binder has been limited by its tendency to cause
hypercalcemia. Since standard
dialysate calcium concentrations (3.0-3.5 mEq/l) increase the risk of developing
hypercalcemia with large doses of CaCO3 by inducing positive
calcium balance during
hemodialysis (HD), we compared control of
hyperphosphatemia in 41 HD patients during 4 months each of
aluminum hydroxide (Al(OH)3) and CaCO3 when the
dialysate calcium concentration was lowered, as required, to maintain the predialysis serum
calcium concentration within the normal range. Mean predialysis serum
phosphorus and
calcium concentrations were 5.0 +/- 0.2 mg/dl and 9.3 +/- 0.1 mg/dl, respectively, during 4 months CaCO3 (9.2 +/- 0.3 g/day) and 4.9 +/- 0.2 g/dl and 9.1 +/- 0.1 mg/dl during the previous 4 months Al(
OH)3
therapy (2.9 +/- 0.2 g/day). Reducing the
dialysate calcium concentration to below 3.0 mEq/l (mean 2.1 +/- 0.04) in the 11 patients who developed
hypercalcemia on CaCO3 decreased serum
calcium (-1.1 +/- 0.15 mg/dl) and ionized
calcium (-0.3 +/- 0.04 mEq/l) during HD, enabled CaCO3 (8.8 +/- 0.4 g/day) to be continued, and maintained predialysis serum
calcium and
phosphorus at 10.4 +/- 0.1 mg/dl and 5.2 +/- 0.3 mg/dl, respectively. No improvement in
acidosis or biochemical
hyperparathyroidism was observed during CaCO3
therapy but serum
aluminum was significantly decreased after CaCO3 (p less than 0.005). We conclude that CaCO3 prevents interdialytic
hyperphosphatemia as effectively as Al(
OH)3 without increasing the predialysis serum
calcium x
phosphorus product, provided serum
calcium is maintained within the normal range by adjusting the
dialysate calcium concentration.