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PHOS-BIND™ - R X Vitamins

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5. Check ionized calcium in 10-14 days following initiation of calcitriol therapy to checkfor hypercalcemia.IMPORTANCE OF SERUM <strong>PHOS</strong>PHORUS CONTROL IN ANIMALSIt has long been recognized that regulation of blood ionized calcium is vital to health.There are a number of hormones and regulators that maintain adequate calcium levels inthe body. Several of these hormones and regulators also have an important impact uponphosphorus levels.In the past ~10 years a specific class of hormones (phosphatonins) has been discovered.The role of these phosphatonins is primarily to keep serum phosphorus from getting toohigh. These mechanisms of action have been the subject of numerous studies. (3, 6,)The results of these studies have helped us understand that maintaining normal serumphosphorus levels and thus preventing hyperphosphatemia is critical with respect to thehealth of the body. Additionally, these studies into phosphatonin activity have shown thatintestinal phosphate binders, such as Phos-Bind, are essential for use in the uremicpatient.CALCITRIOL BENEFITS1. Down-regulates PTH gene to reduce serum parathyroid hormone (PTH)a. Blocks synthesis of PTH within the parathyroid gland by preventingtranscription of the PTH gene onto mRNA.2. Induces synthesis of the calcium receptor that is required to block the secretion of PTHas well as the calcitriol receptor (VDR) in the parathyroid gland (PTG)3. Prevents parathyroid gland hyperplasia during uremia4. Causes regression of the parathyroid gland from its hyperplastic state in the uremicpatient5. Comprehensive listing of additional benefits of calcitriol are found on Table 1 in thereview article by Galvao et al, 2013.6. The CKD patient administered calcitriol will have both a reduction in azotemia and asubstantial decline in the rate of progression of the renal lesions. These benefitsoccur by several mechanisms of action, including the lowering of PTH levels bythe calcitriol.7. Clinical studies and clinician observations confirm that CKD patients receivingcalcitriol supplementation have significantly prolonged survival times andsubstantially improved quality of life.CAUSES OF LOWERED CALCITRIOL1. In CKD the reduced number of functioning renal tubules reduces the synthesis ofendogenous calcitriol.2. High concentrations of serum phosphorus inhibit 1-hydroxylation of 25-hydroxyvitamin D. Serum phosphorus levels can be so high as to actually stop thesynthesis of calcitriol.3. Serum levels of a phosphatonin, Fibroblast Growth Factor 23, (FGF23) are increasedby serum phosphorus. FGF23 is a critical and powerful early suppressor of renalcalcitriol formation.NOTE: Aluminum hydroxide (Phos-Bind) has proven itself to be a safe, convenientand economical way to manage dietary intake of phosphorus in the CKD patient,especially when used concurrently with calcitriol.Phos-Bind 2013 3

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