Calcium citrate, a nonaluminum-containing phosphate-binding agent for treatment of CRF

Abstract

Calcium citrate was evaluated as a dietary phosphate binder in 81 patients with end-stage renal disease. These patients were grouped as follows: Group 1, 43 patients who were treated with calcium citrate; and Group 2 (the control group), 38 patients who were treated with aluminum-containing compounds. Blood chemistries were measured monthly and medications adjusted to maintain the following levels: serum calcium, >9 ml/dl; serum phosphorus, <5.5 mg/dl; and total CO2 content, >22 mmol/liter. At the end of the treatment period, the following serum values were obtained in Groups 1 and 2, respectively: calcium, 9.6 ± 1.2 mg/dl (mean ± SD) versus 8.9 ± 0.8 mg/dl (P < 0.001); phosphorus 5.5 ± 1.9 ml/dl versus 7.0 ± 2.3 mg/dl (P < 0.005); and calcium-phosphate product, 52 ± 18 versus 61 ± 21 (P < 0.05). Differences in alkaline phosphatase, total CO2 content, and C-terminal parathyroid hormone (C-PTH) values were not statistically significant between the two groups. Fifteen patients in Group 1 wer then switched to aluminum-containing compounds and chemistries were compared one month later. During calcium citrate therapy, serum calcium was significantly higher, while C-PTH and serum alkaline phosphatase were significantly reduced. No difference was noted in serum phosphorous and total CO2 content. A questionnaire completed by 17 patients in Group 1 documented excellent patient tolerance to calcium citrate. Hypercalcemia (>10.5 mg/dl) was the only significant complication, but only one patient became symptomatic. We conclude that, as a phosphate binder, calcium citrate is at least as effective as aluminum-containing compounds.