In this article [Kirschbaum, 1998: (http://www.ncbi.nlm.nih.gov/pubmed/9487238)], Kirschbaum (1998) noted that the large dosages (15-23 grams of phosphate, given once or twice a day, in many cases) of dibasic and monobasic sodium phosphate can cause acidosis, in part, because the ratio of H2PO4(-) (monobasic) to HPO4(2-) (dibasic) in some sodium phosphate preparations can be 0.19, and that contrasts with the ratio of H2PO4(-)/HPO4(2-) of 4:1 (or 4) that normally exists in the extracellular fluid in vivo at pH 7.4 (Kirschbaum, 1998). Kirschbaum (1998) argued that the administration of large amounts of sodium phosphate preparations that exist in that type of "acidifying" ratio of monobasic/dibasic phosphate species will "consume" bicarbonate because of the normally-acidic pH of the urine (Kirschbaum, 1998 gives a figure of 6.0, and the urinary pH can be as low as 4.0-4.5). So it's both the relatively high amount of the "acidifying" species [H2PO4(-)] and the high rate at which that species enters the extracellular fluid that has the potential to cause severe problems. The elevation in the anion gap means that there's more phosphate (an unmeasured anion, meaning one that is measured, in a blood test, but not used to calculate the anion gap) relative to bicarbonate (a "measured" anion that's used in the anion-gap calculation), because the acid from the H2PO4(-) has neutralized some of the bicarbonate. MacKay and Oliver (1935) [MacKay and Oliver, 1935: (http://jem.rupress.org/cgi/reprint/61/3/319.pdf)(http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2133223)] noted that supplemental NaH2PO4 or KH2PO4 (monobasic sodium phosphate or potassium phosphate) was likely to have been acidifying and that Na2HPO4 or K2HPO4 was likely to have been alkalinizing. I've seen articles, however, showing that derangements in phosphate homeostasis can be associated with much less predictable disturbances in the serum osmolarity and in acid-base homeostasis.
I scaled the dosages used in that article by MacKay and Oliver (1935), and the "control diet" provided the rats with a dosage of phosphate that scales to a human dosage of 4873 mg of phosphate per day. The dosages that were used to cause kidney damage in the rats were 5-10 times that dosage. I've done scaling calculations for a few articles that actually list the molecular formulas (such as HPO4, etc.) of the dietary supplements and constituents used in animals (that makes me more confident that phosphate means phosphate and not phosphorus, etc.), and the numbers I've gotten have generally agreed with the numbers that Heaney (2004) [Heaney, 2004: (http://www.mayoclinicproceedings.com/content/79/1/91.full.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/14708952), discussed here: (http://hardcorephysiologyfun.blogspot.com/2009/08/more-about-phosphate-metabolism.html)] came up with, in his comparisons of animal and human dosages. The amounts of phosphate in the baseline, control diets (unsupplemented with phosphate) of animals tend to be comparable to a scaled human dosage 4000-6000 or more mg/day.
But one thing to consider is that there might just be some time required to adjust to the acid-base effects of something like Na2HPO4, which is in that supplement I mentioned, or another source of phosphate (even phosphate in milk). A lot of the articles on milk-alkali syndrome discuss acid-base changes in very vague terms, but there are lots of articles showing that the consumption of massive amounts of milk can produce alkalosis and other acid-base disturbances. I'm not sure how clear it is that the phosphate in milk contributes to those effects, but it's a possibility, in my opinion.
But the point is that there's no downside to gradually increasing the dosage of a source of exogenous phosphate, to allow time for the kidneys and other cells to adjust to the changes, etc. That's one reason I don't think the intermittent "phosphate loading" approach is a good idea. One of the articles I discussed in a recent posting shows that 2-3 days can be required for cells in the kidneys and other organs to adjust to an increase in the phosphate intake. Most people probably wouldn't be aware of or require much of a period of time to re-establish normal serum and extracellular fluid electrolyte levels, etc., in response to an increase in phosphate intake [i.e. for decreases in the densities of phosphate transporters on the luminal (apical) membranes of proximal tubule epithelial cells to occur, leading to an increase in phosphate excretion], but one strategy would be to dissolve the source of phosphate in water and drink fractionated amounts of it, as discussed by Giesecke, 1990 [discussed here, by me: (http://hardcorephysiologyfun.blogspot.com/2009/03/enhancing-safety-and-minimizing.html)]. If a person has kidney disease or liver disease or any disease state, however, it would be worthwhile to exercise extra caution, even after discussing these things with one's doctor. One thing that leads me to suggest the potential need to allow time for those types of acid-base homeostatic changes to occur, in the context of an increase in the phosphate/calcium ratio in one's diet, etc., is that I was noticing the striking overlap of the symptoms that can accompany hypophosphatemia (in the context of parenteral nutrition, etc.), in case reports I've been reading, and the side effects that can accompany phosphate supplementation. One way of interpreting that overlap would be to say that the cells in the kidneys and other organs have become adapted to low intracellular phosphate levels and cannot immediately respond to an acute increase in phosphate availability. So the parenteral nutrition acutely drives phosphate into cells and can sometimes cause acute hypophosphatemia with electrolyte abnormalities [producing the "pedal edema," or edema in the feet, plasma volume expansion, or dyspnea (shortness of breath), etc.], and phosphate supplements have the potential to produce the same electrolyte abnormalities and abrupt increase in intracellular phosphate. And both hyperphosphatemia and phosphate supplementation have sometimes been associated with pedal edema or plasma volume expansion, dyspnea, etc. The overlap of the symptoms associated with phosphate depletion and phosphate "excess" is considerable, in my opinion, and has the potential to create confusion. Also, pedal edema is known to be associated with congestive heart failure, and researchers have found that a reversible form of congestive heart failure can occur in some people who have hypophosphatemia [Darsee and Nutter, 1978: (http://www.ncbi.nlm.nih.gov/pubmed/363007)]. To the extent that an exogenous source of phosphate could produce transient plasma volume expansion, the tendency could be to erroneously attribute transient derangements in electrolytes or in acid-base markers to pathological effects of phosphate. In other cases, however, some of the derangements might be correctly attributable to pathological effects of phosphate. I'm just saying that the presumed "hypersensitivity" of mechanisms aimed at phosphate retention, in the context of chronic phosphate depletion, would suggest the need for making gradual changes, if any, under a doctor's supervision, especially past a certain point or in people in disease states.
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