More on phosphate - kidney - vitamin D stuff

Discussion in 'Other Research' started by Not dead yet!, Feb 19, 2018.

  1. Not dead yet!

    Not dead yet! Well-Known Member

    Not for the first time, I'm up at night after having gone to bed heavily medicated due to a migraine that hits when I get my period. It also happens at the exact same time as my kidneys just stop working. Not scanty urine, not "can't go" but none at all is produced for about 18 to 24 hours. Then when it is produced, it smells like a skunk (part of me, the part that ignores pain is looking for a joke there about old genetics and Neanderthals, but I'll skip it). :p

    Anyway, this pattern has been true since I was 20 when my migraines started. I've mentioned it to no less than 30 doctors, not one of them did more than shrug, not even neurologists or gyno's.

    So not for the first time, I'm searching pubmed for why this happens. This time I might have found something interesting:

    Article: From the Perspectives section (the "Conclusions" in this case):

    Even relatively small elevations of serum phosphorus in the high normal range have been correlated in observational studies with increased cardiovascular and all cause mortality in patients with CKD13, diabetes14, coronary artery disease15, or even normal adults16. Phosphate load may be an important driver of vascular calcification, even in the absence of overt hyperphospahatemia5,8,9.

    High serum levels of FGF23 have been associated with increased left ventricular mass17, increased arterial stiffness18 and more rapid decline of renal function19, although its relation with vascular calcification remains rather conflicting10. It should be noted that in all these studies the effect of FGF23 was independent of serum phosphate levels indicating that perhaps FGF23 is superior to serum phosphorus levels as a marker of morbidity or mortality in CKD patients10, 20.

    As vitamin D increases FGF23 levels it would sound logical that this kind of therapies might be detrimental for CKD patients. However there are conflicting data, as increased FGF23 serum levels have been associated with increased mortality, whereas vitamin D treatment have been associated better survival in HD patients. Wolf has offered many explanations on this paradox10.

    Current recommendations from various authorities suggest that serum phosphorus levels should be maintained between 2.7- 4.7 mg/dl in patients with CKD 3-4 and 3,5-5,5 mg/dl in CKD 5 via dietary phosphorus restriction or therapy with phosphate binders1,2. Although previous studies have shown a beneficial effect of a low in phosphorus diet, recent data indicate that this approach is frequently accompanied by an excessive risk of malnutrition and should be avoided21.

    The studies regarding therapies with phosphate binders have mainly focused in dialysis patients and there are only a few studies with a limited number of patients in CKD 3-4 patients with sevelamer hydrochloride22, sevelamer carbonate23 of lanthanum carbonate24.

    Recently, Isakova et al raised doubts regarding the "optimal" levels of serum phosphorus, as they were based mainly on observational studies with many methodological limitations and there is a need for new well designed multicenter studies with adequate patient populations20. They also proposed a possible role for FGF23 as a marker of hyperphosphatemia equal to that of glycosylated hemoglobin in diabetes mellitus, as its levels remain rather stable over long time periods and as a marker of the possible favorable response to vitamin D analogues in severe secondary hyperparathyroidism, or to phosphate binders administration even in patients with serum phosphorus levels among the "normal' levels (2.7- 4.7 mg/dl).


    In another place, I saw something about the use of ferric citrate as a phosphate binder. Being someone who remembers stuff she learned in chemistry class, I noticed that most supplements say "iron citrate" not "ferric citrate." And that reminded me that there is a difference between ferric (+3) and ferrous (+2). Well ok, I had to look up the +, but I knew they were off by 1. :D

    So when I pushed google on that point, I came up with a clinical trial ongoing about this:https://clinicaltrials.gov/ct2/show/NCT02888171

    Basically they suspect that ferric iron is better used by the body and doesn't go into instant storage.

    Does the ferric version of iron exist as a supplement? Is there either a ferric citrate or ferric gluconate or whichever, as long as it's the ferric form? So far I haven't found one. But it could solve so much for me. It might explain a lot about why my body "ignores" Vitamin D3. I might have mentioned before that only D2 is converted to active D reliably by my body.

    The pain relieving effect of proper vitamin D levels are the difference between life and undeath for me, so I"ll keep looking.
     
  2. Not dead yet!

    Not dead yet! Well-Known Member

    Hmm, this looks interesting:
    Article: Abstract

    From chronic kidney disease (CKD) Stage 4 onwards, phosphate binders are needed in many patients to prevent the development of hyperphosphataemia, which can result in disturbed bone and mineral metabolism, cardiovascular disease and secondary hyperparathyroidism. In this review, we re-examine the use of magnesium-containing phosphate binders for patients with CKD, particularly as their use circumvents problems such as calcium loading, aluminum toxicity and the high costs associated with other agents of this class. The use of magnesium hydroxide in the 1980s has been superseded by magnesium carbonate, as the hydroxide salt was associated with poor gastrointestinal tolerability, whereas studies with magnesium carbonate show much better gastrointestinal profiles. The use of combined magnesium- and calcium-based phosphate binder regimens allows a reduction in the calcium load, and magnesium and calcium regimen comparisons show that magnesium may be as effective a phosphate binder as calcium. A large well-designed trial has recently shown that a drug combining calcium acetate and magnesium carbonate was non-inferior in terms of lowering serum phosphate to sevelamer-HCl and had an equally good tolerability profile. Because of the high cost of sevelamer and lanthanum carbonate, the use of magnesium carbonate could be advantageous and drug acquisition cost savings would compensate for the cost of introducing routine magnesium monitoring, if this is thought to be necessary and not performed anyway. Moreover, given the potential cost savings, it may be time to re-investigate magnesium-containing phosphate binders for CKD patients with further well-designed clinical research using vascular end points.
     
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