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deteriorating renal function could possibly overwhelm the capacity of the physiological inactivation mechanism that ordinarily controls the bioactive FGF-23 concentrations. It has been reported that increased production of FGF-23 by the bone may contribute to elevated levels in CKD and ESRD. 4,5 However, the biologic activity of C-terminal FGF-23 fragments remains a controversial topic and the mechanism postulated to explain the reduced renal clearance or decreased degradation rate of C terminal FGF-23 in CKD remains unclear.
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Kavita Shalia (2017) studied this question.
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