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      Long-Term (6 Months) Cross-Over Comparison of Calcium Acetate with Calcium Carbonate as Phosphate Binder

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          A previous short-term study of 10 weeks in 8 patients had shown us that with half the dose of elemental calcium, calcium acetate (CaAc) could control predialysis plasma phosphate (PPO<sub>4</sub>) as well as calcium carbonate (CaCO<sub>3</sub>) but that the incidence of hypercalcemia was not decreased. To better appreciate the value of CaAc in comparison to CaCO<sub>3</sub>, CaAc was given to 28 patients on chronic hemodialysis (6 men, 22 women, age 61 ± 14 years; dialyzate Ca: 1.5 mmol/l) for 6 months to replace CaCO<sub>3</sub> at half the dose of elemental calcium (1,235 ± 521 versus 2,375 ± 1,470 mg/day). Because of gastrointestinal intolerance, CaAc had to be discontinued in 5 patients after 1-5 months. Magnesium hydroxide [Mg(OH)<sub>2</sub>] given in 18 of them in association with CaCO<sub>3</sub> was discontinued and reintroduced in 6 patients in order to keep PPO<sub>4</sub> < 2 mmol/l. Mean dosage of Mg(OH)<sub>2</sub> was 2.09 ± 1.4 g/day with CaCO<sub>3</sub> and 0.9 ± 0.5 with CaAc. Predialysis plasma concentrations of calcium and phosphate were monitored weekly during the 3 months of the control period under CaCO<sub>3</sub> and during the 6-month administration of CaAc. Plasma calcium (PCa) was comparable with the 2 treatments (2.47 ± 0.11 vs. 2.5 ± 0.10 mmol/l), but PPO<sub>4</sub> was significantly lower with CaAc (1.82 ± 0.26 vs. 1.73 ± 0.23 mmol/l). Plasma alkaline phosphatase remained constant (122 ± 66 vs. 122 ± 70; normal < 170 UI/l) as well as plasma intact PTH (121 ± 153 vs. 121 ± 146; normal < 54 pg/ml) and plasma aluminum (0.34 ± 0.23 vs. 0.32 ± 0.20 μmol/l). Hypercalcemia (PCa > 2.7 mmol/l) was present in 11 patients with CaCO<sub>3</sub> and in 16 patients with CaAc, and its incidence did not decrease with CaAc (8.2 vs. 8%). In conclusion, this long-term study confirms that CaAc is a more efficient PO<sub>4 </sub>binder than CaCO<sub>3</sub>. However, its gastrointestinal tolerance seems poorer and the incidence of hypercalcemia is not decreased. The paradox of the unchanged incidence of hypercalcemia with acetate in spite of a reduction by half of the amount of calcium ingested may have two explanations: the very presence of a lower plasma PO<sub>4</sub> concentration (by a physicochemical mechanism) and the possible greater bioavailability of the calcium for absorption when it is given as CaAc.

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          Author and article information

          S. Karger AG
          12 December 2008
          : 63
          : 3
          : 258-262
          Service de Néphrologie, CHU Amiens, France
          187207 Nephron 1993;63:258–262
          © 1993 S. Karger AG, Basel

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          Page count
          Pages: 5
          Original Paper

          Cardiovascular Medicine, Nephrology

          Phosphate binder, Calcium acetate, Calcium carbonate


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