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Journal ArticleDOI

Effect of the time of administration of calcium acetate on phosphorus binding.

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TLDR
It is concluded that calcium acetate increases fecal excretion of phosphorus by binding both dietary and endogenous phosphorus, but the binding of dietary phosphorus is quantitatively much more important.
Abstract
Phosphorus binders are given to patients with renal failure to increase gastrointestinal excretion of phosphorus. To determine the relative importance of the binding of dietary as compared with endogenous phosphorus and to determine the optimal dose schedule, we gave either 4.4 g of calcium acetate (25 mmol of calcium) or a placebo to six normal subjects on each of seven different schedules in a randomized sequence. The net gastrointestinal balance of phosphorus and calcium was determined by a one-day lavage technique. After a meal containing approximately 12 mmol of phosphorus, the mean phosphorus absorption (+/- SE) measured 9.17 +/- 0.36 mmol (78 percent) with placebo but decreased to 3.81 +/- 0.58 mmol (31 percent) when calcium acetate was given immediately before the meal (representing binding of 5.36 +/- 0.77 mmol of phosphorus). Similar binding was observed when calcium acetate was given immediately after the meal and when half the dose was given before and half after the meal. In contrast, when calcium acetate was given two hours after the meal or while the subject was fasting, phosphorus binding was reduced to 2.00 +/- 0.52 mmol and 1.81 +/- 0.84 mmol, respectively. Calcium absorption from calcium acetate averaged 21 +/- 1 percent when the binder was given with a meal; absorption from calcium acetate averaged 40 +/- 4 percent when the binder was given while the subject was fasting. We conclude that calcium acetate increases fecal excretion of phosphorus by binding both dietary and endogenous phosphorus, but the binding of dietary phosphorus is quantitatively much more important. For the most efficient phosphorus binding, calcium (and presumably other phosphorus-binding cations) should be given with meals.

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Dietary Reference Intakes

TL;DR: The development of DRIs replaces the periodic revisions of Recommended Dietary Allowances (RDAs), which have been published since 1941 by the National Academy of Sciences.
References
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Journal ArticleDOI

The dialysis encephalopathy syndrome. Possible aluminum intoxication.

TL;DR: The fact that brain gray-matter aluminum was higher in all patients with the dialysis-associated encephalopathy syndrome than any of the control subjects or other uremic patients on dialysis suggests that this syndrome may be due to aluminum in intoxication.
Journal ArticleDOI

Calcium Carbonate as a Phosphate Binder in Patients with Chronic Renal Failure Undergoing Dialysis

TL;DR: Calcium carbonate successfully lowered serum phosphorus levels and raised serum calcium levels in the majority of the authors' patients, thereby confirming that this agent may be a satisfactory substitute for traditional phosphate binders that contain aluminum.
Journal ArticleDOI

Bone Aluminum and Histomorphometric Features of Renal Osteodystrophy

TL;DR: Findings are consistent with but do not prove the hypothesis that aluminum plays a pathogenic role in dialysis osteomalacia; the mechanism by which aluminum accumulates remains unknown.
Journal ArticleDOI

Reduction of dietary phosphorus absorption by phosphorus binders. A theoretical, in vitro, and in vivo study.

TL;DR: Cal calcium acetate, not previously used for medical purposes, is approximately as efficient as aluminum carbonate gel and more efficient as a phosphorus binder than other currently used calcium salts.
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