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Role of Calcium Carbonate Administration Timing in Relation to Food Intake on Its Efficiency in Controlling Hyperphosphatemia in Patients on Maintenance Dialysis
Author(s) -
Sechet A.,
Hardy P.,
Hottelart C.,
Rasombololona M.,
Abighanem O.,
Oualim Z.,
Brazier M.,
Achard J.M.,
Pruna A.,
Moriniere P.,
Fournier A.
Publication year - 1998
Publication title -
artificial organs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 76
eISSN - 1525-1594
pISSN - 0160-564X
DOI - 10.1046/j.1525-1594.1998.06199.x
Subject(s) - hyperphosphatemia , chemistry , calcium , bicarbonate , parathyroid hormone , medicine , urea , creatinine , dialysis , endocrinology , meal , phosphate , crossover study , biochemistry , food science , placebo , alternative medicine , pathology
A study has claimed that at an equal elemental calcium dose, CaCO 3 was not less but equally as efficient in controlling predialysis hyperphosphatemia as calcium acetate, provided both calcium salts were ingested 5 min before meals instead of during meals because the higher acidity of the fasting gastric juice would allow for better dissociation of CaCO 3 . However, this study did not directly demonstrate that the efficiency of CaCO 3 in controlling hyperphosphatemia was actually greater when it was administered before a meal than during a meal. To examine this point, we performed a 3 month randomized crossover trial in 12 reliable and stable patients maintained on chronic hemodialysis. Their plasma concentrations of calcium, protein, phosphate, bicarbonate, urea, and creatinine were measured before the first dialysis of each week and the amount of intact parathyroid hormone (PTH) at the beginning and at the end of each of the 3 months. Comparison of the plasma concentrations measured during the 2 modes of administration showed no significant differences in creatinine, urea, bicarbonate, or intact PTH. The mean (±SD) plasma concentration of PO 4 was not significantly lower (1.88 ± 0.50 vs. 1.74 ± 0.41 m M ) whereas the corrected level of plasma Ca was significantly lower (2.30 ± 0.17 vs. 2.38 ± 0.16 m M ; p < 0.04) when CaCO 3 was given before meals than during meals. In conclusion, the administration of CaCO 3 before a meal does not increase its efficiency in controlling hyperphosphatemia because the level of plasma PO 4 was actually slightly higher with this timing of administration whereas the comparison of the creatinine and urea levels suggested a stability of phosphate intake and the comparison of the PTH and bicarbonate levels suggested the stability of osteolysis and of the transcellular membrane shift of phosphate. Also, administration of CaCO 3 before a meal is associated with significantly lower plasma corrected calcium, suggesting less absorption of calcium, which may be an advantage but only in hypercalcemic patients. There is no reason other than the prevention of its hypercalcemic effect to recommend the administration of CaCO 3 just before meals rather than during meals.

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