BACKGROUND: The increasing use of 'reduced calcium' dialysate in CAPD patients treated with calcium-based phosphate binders has raised concerns that this could lead to negative calcium balance, worsening hyperparathyroidism, and osteopenia. METHODS: The present study was conducted to examine the possibilities (a) that 1.25 mM calcium dialysate leads to negative calcium balance and worsening hyperparathyroidism, and (b) that conversely 1.25 mM calcium dialysate is still too high for some patients. We studied 22 patients who, after a 2-month run in using 1.75 mM calcium dialysate and aluminium hydroxide binders, entered a 3-month phase of 1.25 mM calcium dialysate with continuation of aluminium hydroxide as the sole phosphate binder. The patients then entered a final 9-month phase in which dialysate calcium remained at 1.25 mM and calcium carbonate was substituted for aluminium hydroxide and progressively titrated to achieve optimum phosphate control. RESULTS: During the initial 3-month period, parathyroid hormone increased from 259, range 11-1149 to 405, range 16-1318 pg/ml (P = 0.0001) and ionized calcium decreased from 1.17 +/- 0.06 to 1.11 +/- 0.08 mM (P = 0.0004). The subsequent 9-month phase was associated with return of parathyroid hormone to baseline levels. Further dialysate calcium reduction to 0.6 mM was implemented in the four patients who became hypercalcaemic. CONCLUSION: This study has clearly shown that reduction of dialysate calcium to 1.25 mM can be harmful to CAPD patients if oral calcium availability is inadequate. It has also shown that dialysate calcium at 1.25 mM is a compromise, with increased risk of hyperparathyroidism if calcium intake is too low and, conversely, risk of hypercalcaemia and unacceptable increases of the Ca x Pi product in a minority of patients. At these extremes there is a need for a high-calcium dialysate (1.75 mM) and a very low-calcium dialysate (0.6 mM or less), to optimize management.
BACKGROUND: The increasing use of 'reduced calcium' dialysate in CAPD patients treated with calcium-based phosphate binders has raised concerns that this could lead to negative calcium balance, worsening hyperparathyroidism, and osteopenia. METHODS: The present study was conducted to examine the possibilities (a) that 1.25 mM calcium dialysate leads to negative calcium balance and worsening hyperparathyroidism, and (b) that conversely 1.25 mM calcium dialysate is still too high for some patients. We studied 22 patients who, after a 2-month run in using 1.75 mM calcium dialysate and aluminium hydroxide binders, entered a 3-month phase of 1.25 mM calcium dialysate with continuation of aluminium hydroxide as the sole phosphate binder. The patients then entered a final 9-month phase in which dialysate calcium remained at 1.25 mM and calcium carbonate was substituted for aluminium hydroxide and progressively titrated to achieve optimum phosphate control. RESULTS: During the initial 3-month period, parathyroid hormone increased from 259, range 11-1149 to 405, range 16-1318 pg/ml (P = 0.0001) and ionizedcalcium decreased from 1.17 +/- 0.06 to 1.11 +/- 0.08 mM (P = 0.0004). The subsequent 9-month phase was associated with return of parathyroid hormone to baseline levels. Further dialysate calcium reduction to 0.6 mM was implemented in the four patients who became hypercalcaemic. CONCLUSION: This study has clearly shown that reduction of dialysate calcium to 1.25 mM can be harmful to CAPD patients if oral calcium availability is inadequate. It has also shown that dialysate calcium at 1.25 mM is a compromise, with increased risk of hyperparathyroidism if calcium intake is too low and, conversely, risk of hypercalcaemia and unacceptable increases of the Ca x Pi product in a minority of patients. At these extremes there is a need for a high-calcium dialysate (1.75 mM) and a very low-calcium dialysate (0.6 mM or less), to optimize management.