In their in vitro experiments at physiological pH values, Sheikh et al. (1989) [Shiekh et al., 1989: (http://www.pubmedcentral.nih.gov/picrender.fcgi?pmid=2910921&blobtype=pdf)(http://www.ncbi.nlm.nih.gov/pubmed/2910921)] found that calcium (Ca2+) acetate was more effective in binding phosphate (Pi) than calcium carbonate was, and the authors also found that magnesium (Mg2+) was less effective than calcium in binding phosphate in vitro. However, Spiegel et al. (2007) [Spiegel et al., 2007: (http://www.ncbi.nlm.nih.gov/pubmed/17971314)] cited research (reference 10, cited on p. 421) in which the authors had made the argument that Mg2+ is likely to bind more phosphate than Ca2+ in vivo, primarily because less Mg2+ is going to be absorbed than Ca2+. I think that argument is likely to be valid, and the main thing would be to try to separate the administration of supplemental Mg2+ from the administration of Pi by at least 2 hours [Heaney, 2004: (http://www.mayoclinicproceedings.com/content/79/1/91.full.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/14708952)]. But the significance of the in vitro comparison of Ca acetate and Ca carbonate is that those experiments (Shiekh et al., 1989) provide an indirect explanation of one mechanism by which so-called Pi binders, including Ca alpha-ketoglutarate, reduce serum Pi in vivo. The mechanism is the formation, in the intestinal lumen, of heterogeneous precipitates (a.k.a. epitaxial growth of precipitates, heterotopic crystallization, etc.) that are amorphous or crystalline in their structures and that are composed of one or more anionic species, including urate or oxalate or ketoglutarate or other dicarboxylic acids (or even unconjugated bilirubin or bile salts, etc.) and Ca or Mg or both [(http://scholar.google.com/scholar?hl=en&q=epitaxial+phosphate+calcium)]. I should mention that the sequestration of Pi in the intestinal tract can't explain the reductions in serum Pi that the parenteral administration of amino acids has sometimes produced (http://hardcorephysiologyfun.blogspot.com/2009/09/reductions-in-serum-phosphate-induced.html). The reason is that the amino acids were administered parenterally and not enterally (i.e. jejunally or duodenally or orally or whatever variation on that). In any case, these are some of the articles showing the serum Pi-lowering effect of Ca alpha-ketoglutarate [Birck et al., 1999: (http://ndt.oxfordjournals.org/cgi/reprint/14/6/1475.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/10383011); (http://scholar.google.com/scholar?hl=en&q=calcium+ketoglutarate+phosphate+binder)], and I don't think much of those calcium salts of organic anions as Pi binders or of Ca supplements in general. But it's interesting that bilirubin can form heterogeneous precipitates with Ca Pi, and "Ca Pi" supplementation decreased plasma bilirubin without altering the rates of urinary calcium or phosphate excretion [Van der Veere et al., 1997: (http://www.ncbi.nlm.nih.gov/pubmed/9024299)]. These are some other articles that show that effect (http://scholar.google.com/scholar?hl=en&q=calcium+phosphate+bilirubin).
Those mechanisms could mean that reasonable but not excessive intakes of Pi could serve to increase or "maintain" the excretion of bilirubin, but higher dosages could produce more of a nucleating effect and produce cholelithiasis (gallstones composed of mixed Ca and Mg precipitates of urate and phosphate, etc.). In the context of purine nucleotide supplementation, small changes in the ratios of phosphate, derived from nucleotide monophosphates or triphosphates, to exogenous-nucleotide-derived urate and xanthine could influence the formation of those types of precipitates. Adenosine that reaches the liver could increase Pi uptake by sequestering Pi in purine nucleotides and by increasing the activities of phosphofructokinase and other glycolytic enzymes, but an increase in biliary urate excretion (a significant amount can be excreted in the bile, rather than the urine), as a result, could increase the formation of heterogeneous precipitates with Ca Pi in the common bile duct and cause a biliary obstruction, etc. Those types of interactions would probably not be significant at most dosages, in my opinion, but it's potentially useful to be aware of that type of thing. That type of "extreme" scenario would be unlikely in anyone who is using reasonable dosages but could be more likely to occur in a person who is diabetic or insulin-resistant, for example.
It's interesting that the absorption of Mg, in particular, can also be drastically decreased by its binding to and sequestration by bile acids and unabsorbed fatty acids in people who display malabsorption due to liver disease, etc., and I've cited research on that in past postings. The dosages of Mg that researchers had to use to overcome that binding effect and just correct the deficiency state, in children who were undergoing treatment for liver disease, works out to a dose of 2380 mg/day of Mg for a 70-kg human [Heubi et al., 1997: (http://www.ncbi.nlm.nih.gov/pubmed/9285381); (http://hardcorephysiologyfun.blogspot.com/2009/01/articles-on-pantothenic-acid-vitamin-b5.html)]. That means that most of that 2,380 mg (or equivalent dosages in children) was not even available for absorption. And those children weren't even having to consider the binding of Mg by phosphate, etc. There's actually a scaling factor of about 2 that's sometimes used to convert children's dosages to adults' dosages, but I think that scaling factor is only applicable to children within a fairly narrow range of ages. But even supposing it's 1,190 mg of Mg that's being bound by endogenous bile salts and dietary fatty acids in an adult who has liver disease, it's relevant that as many as 20-30 percent of Americans display some degree of nonalcoholic fatty liver disease. A gram of phosphate can bind up to 1800 mg of Mg. That means the intake of a person who is not taking supplemental Mg and who is adding a gram of phosphate to his or her diet, through meat intake or some other route, could conceivably be receiving a daily Mg intake of "negative 2690 mg," assuming the person gets the usual, measly 300 mg/day from foods. In reality, the Pi wouldn't bind that much Mg in vivo, especially if the Mg were taken at a different time. But the point is that the magnitude of the Mg binding can be very large, and the nucleating effect of some of these endogenous, anionic compounds could create complex dose-response relationships for something like Pi. The formation of heterogeneous precipitates of bilirubin and calcium phosphate could also explain the apparent "phosphate-sparing" effect of calcium phosphate, even though calcium phosphate is more or less insoluble (see Heaney, 2004). (The calcium phosphate could remain insoluble and promote the nucleation of complexes of calcium and bilirubin, thereby reducing the amount of calcium that would be available to bind to dietary phosphate. That could increase the amount of phosphate that would be available for absorption. I don't quite understand the stoichiometries of the binding of soluble calcium with bilirubin and calcium phosphate or magnesium phosphate to form insoluble, heterogeneous precipitates, but it's likely that no one understands those issues.)
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