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Keryx Biopharmaceuticals Inc. Message Board

  • kerx4sale kerx4sale Feb 13, 2013 10:21 AM Flag

    Phosphate and FGF-23 by Harald Juppner

    just google and make up your mind

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    • I am not a medical professional and not a bio-chemist, just an investor who read bio papers for personal gains, so take it for what it is...the FGF-23 is a parameter to gauge a kidney functionality as to how it handles phosphorus, phosphate binders are not designed to directly improve kidney functionality, thus FGF-23 should be looked at as secondary parameter..certainly phosphate binders may somewhat improve or stabilize kidney functionality over time due to reduction of phosphorus level and thus less mineralization/degradation of kidneys, and this may have good impact on FGF-23 at early stages of CKD (in late stages kidneys already gone, and there is no help), but this is indirect impact..thus I think FGF-23 is less relevant in testing of phosphate binders...

    • Can somebody explain how this article relates to KERX for somebody who does not make a living in a lab?

      Thanks in advance.

      Sentiment: Hold

    • Thanks. Seems the response of FGF response is biphasic. In early/mild CKD and most certainly in normophosphatemia, FGF-23 helps regulate phosphate levels (unclear which stages this relates to; my lab does not have access to nephrology journals). As kidney disease progresses (Stage 3? Stage 4? Stage 5?) FGF starts to go through the roof where the association between FGF levels and assistance in eliminating phosphate is lost…even though FGF-23 is biologically active. As stated in the paper, there appears to be no clear relationship between overall patient outcomes and reducing FGF-23 levels. As such, FGF-23 may be a very good marker for kidney disease at all stages, but I do not see how FGF-23 levels will signal benefits of phosphate binding particularly in the later stages of CKD and most certainly in ESRD.


    • Thanks, very informative!

      Abstract from a 2011 Nature article:

      Fibroblast growth factor (FGF)-23 is probably the most important regulator of serum phosphate and calcitriol (1,25(OH)2D3) levels. It is secreted by osteocytes and osteoblasts in response to oral phosphate loading or increased serum 1,25(OH)2D3 levels. In human chronic kidney disease (CKD), plasma FGF-23 appears to be a sensitive biomarker of abnormal renal phosphate handling, as FGF-23 levels increase during early stages of kidney malfunction. In humans and animals with CKD, elevated FGF-23 levels increase fractional phosphate excretion, reduce serum phosphate levels, and reduce 1α-hydroxylase activity, which reduces 1,25(OH)2D3 formation thereby increasing parathyroid hormone (PTH) secretion. FGF-23 thus has a key adaptive role in maintaining normophosphatemia. Plasma FGF-23 continues to increase as CKD progresses, increasing by orders of magnitude in end-stage renal disease. At the same time, responsiveness to FGF-23 declines as the number of intact nephrons declines, which is associated with reduced expression of Klotho, the co-receptor required for FGF-23 signaling. In late CKD, FGF-23 cannot reduce serum phosphate levels, and abnormally high plasma FGF-23 concentrations appear to exert unwarranted off-target effects, including left ventricular hypertrophy, faster CKD progression, and premature mortality. Lowering serum phosphate levels through the use of oral phosphate binders and/or long-acting PTH agents may reduce FGF-23 levels in early CKD stages, thereby limiting off-target effects, which may improve patient outcomes.

      Sentiment: Strong Buy

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