These articles [Thomas, 1978: (http://www.ncbi.nlm.nih.gov/pubmed/351267); Lau et al., 1979: (http://www.ncbi.nlm.nih.gov/pubmed/44888)] are really good, and Lau et al. (1979) found that the administration of alkaline phosphate preparations [salts of HPO4(2-)] to people who had hypercalciuria, due to either inappropriately-increased intestinal calcium absorption (absorptive hypercalciuria) or renal hypercalciuria (due to some problem originating in the kidneys and causing an excess of urinary calcium excretion), reduced the rate of urinary calcium excretion much more than neutral phosphate preparations or reductions in the subjects' dietary calcium intakes did. Thomas (1978) also noted that alkaline phosphate preparations but not acidic phosphates reduce urinary calcium and do only (or, probably, mainly) in people who are hypercalciuric. Lau et al. (1979) and Thomas (1978) also cited and discussed research showing that oral phosphate preparations increase pyrophosphate excretion and probably inhibit renal calcifications and stone formation, in part, by that mechanism. I don't know what the mechanism is thought to be for that effect, but it's conceivable that it occurs because inorganic phosphate, at concentrations found in vivo, can inhibit alkaline phosphatase activity (a high smooth-muscle-cell alkaline phosphatase activity tends to increase the risk of soft-tissue calcification by breaking down an inhibitor of calcification, namely pyrophosphate, into orthophosphate [HPO4(2-)], which can, at excessive concentrations, contribute to calcification) [Coburn et al., 1998: (http://jcem.endojournals.org/cgi/content/full/83/11/3951)(http://www.ncbi.nlm.nih.gov/pubmed/9814474?dopt=Abstract)]. A low alkaline phosphatase activity on the plasma membranes of various cell types or even in the serum could conceivably increase intracellular PLP, or coenzymated vitamin B6, and reduce extracellular or serum PLP levels, given that some minimal degree of alkaline phosphatase activity is required for cleavage of PLP and, hence, entry of B6 into cells, where it's rephosphorylated. So an excess of phosphate could conceivably cause B6 depletion by impairing B6 entry into cells, but Coburn et al. (1998) noted that phosphate depletion is more likely to reduce (intracellular) PLP levels by reducing the availability of phosphate for the phosphorylation of pyridoxal. It's not a technical statement and wouldn't necessarily be true, but maybe adequate amounts of dietary phosphate increase the ratio of pyrophosphate to orthophosphate in the extracellular fluid, etc. Many articles have shown that phosphate depletion tends to be accompanied by elevated serum alkaline phosphatase activity (http://scholar.google.com/scholar?hl=en&q=hypophosphatemia+%22alkaline+phosphatase%22), and that or tissue-restricted increases in alkaline phosphatase activity could occur in response to dietary phosphate depletion and, up to some point, above which the opposite effect could occur, increase the risk of soft-tissue calcification. I think there's some middle ground. The orthophosphates joined together in pyrophosphate have to come from somewhere. Also, Lau et al. (1979) found that neutral phosphate, in comparison to acidic phosphate [salts of H2PO4(-)], caused a lower rate of net acid excretion in the urine (and, not surprisingly, given that a major acidic species in urine is ammonium, caused a lower rate of ammonium excretion) and a higher rate of urinary citrate excretion. Urinary citrate is thought to protect against calcium phosphate or oxalate precipitation. One way of looking at the difference in acid excretion would be to say that more HPO4(2-) might have been available for protonation and excretion as H2PO4(-) in the group supplemented with neutral phosphate than in the acid phosphate group, thereby reducing renal ammoniagenesis and acid excretion as the ammonium ion [NH4(+)], but that's probably an overly-simplistic explanation.
Lewandowski and Rogers (2004) [Lewandowski and Rogers, 2004: (http://www.ncbi.nlm.nih.gov/pubmed/15232796)] found that 100 mg/day of vitamin B6 reduced urinary calcium, phosphorus (phosphate), and the amount of brushite "supersaturation" in relation to other forms of calcium phosphate crystals or amorphous aggregations. They also found that glutamine supplementation reduced "relative calcium oxalate supersaturation" in the urine, implying that it could help to reduce calcium oxalate stone formation, in theory. Maybe glutamine increased citrate excretion by acting as a precursor to citrate, given that researchers have shown that glutamine can increase the levels of intracellular and intramitochondrial citrate and other TCA cycle intermediates in various cell types. A higher urinary citrate is, as Lau et al. (1979) and others have noted, thought to be protective against calcium stone formation, and Cupisti et al. (2007) [Cupisti et al., 2007: (http://www.ncbi.nlm.nih.gov/pubmed/17184967)] found that insulin resistance was associated with a lower rate of urinary citrate excretion. I think 100 mg/day of vitamin B6 is too high as a long-term dosage of vitamin B6, mainly because of the risk of peripheral neuropathy, and 25-50 mg/day would, in my opinion, be a safer dose, in many cases, in the long term. The authors noted that vitamin B6 could have reduced urinary oxalate by increasing its metabolism (by PLP-dependent enzymes), and the authors didn't know why vitamin B6 had decreased urinary calcium excretion. It's mysterious, and I've discussed past research showing that vitamin B6 supplementation, in animals, can decrease serum calcium levels. That's not desirable, necessarily, when one looks at the many different effects, taken together, of vitamin B6. But there's probably some lower dosage that would be safer in the long term and that might produce some of the reductions in calcification of soft tissues (in addition to the antihypercalciuric effect that it could potentially have) that have also been associated with vitamin B6 supplementation (http://scholar.google.com/scholar?hl=en&q=calcification+%22vitamin+B6%22+OR+pyridoxine). Some of those articles are research on the use of magnesium to prevent calcification, and the authors appear to have just mentioned vitamin B6 or used it in combination with magnesium (MgO is magnesium oxide). Some authors have noted that excessive amounts of dietary phosphate could bind to calcium and thereby indirectly enhance urinary oxalate excretion, given that less oxalate in foods would bind to calcium in the gastrointestinal tract (more would be absorbed and then excreted in the urine). That could be important to remember, but who knows how much oxalate comes from foods or if the problem is more that the oxalate isn't being metabolized (or maybe too much is being formed, as a result of the metabolic syndrome, as suggested by the research of Cupisti et al. (2007), cited above). Sayer et al. (2004) [Sayer et al., 2004: (http://cs.portlandpress.com/cs/106/0549/1060549.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/15027893)] was basically that, following some initial calcium oxalate precipitation (crystal formation), calcium phosphate can be more likely to precipitate and form mixed crystals, I guess, through "heterologous nucleation" (this must mean that there's a seeding effect of the calcium oxalate). Thus, vitamin B6 or glutamine (or whatever other factors that could reduce urinary oxalate supersaturation) could conceivably reduce urinary calcium phosphate deposition, in my opinion. Glutamine is probably not going to produce especially reliable effects, but I just think increases in glutamine availability (or maintenance of its availability) interacts favorably with the metabolic effects of inorganic phosphate, by multiple mechanisms.
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