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      Hyperphosphatemia Management in Patients with Chronic Kidney Disease

      a , * , b

      Saudi Pharmaceutical Journal : SPJ

      Elsevier

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          Abstract

          Hyperphosphatemia in chronic kidney disease (CKD) patients is a potentially life altering condition that can lead to cardiovascular calcification, metabolic bone disease (renal osteodystrophy) and the development of secondary hyperparathyroidism (SHPT). It is also associated with increased prevalence of cardiovascular diseases and mortality rates. To effectively manage hyperphosphatemia in CKD patients it is important to not only consider pharmacological and nonpharmacological treatment options but also to understand the underlying physiologic pathways involved in phosphorus homoeostasis. This review will therefore provide both a background into phosphorus homoeostasis and the management of hyperphosphatemia in CKD patients. In addition, it will cover some of the most important reasons for failure to control hyperphosphatemia with emphasis on the effect of the gastric pH on phosphate binders efficiency.

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          Most cited references 122

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          Relation between serum phosphate level and cardiovascular event rate in people with coronary disease.

          Higher levels of serum phosphate are associated with adverse cardiovascular outcomes, especially in the setting of overt hyperphosphatemia. Given the biological importance of phosphorus, it is plausible that higher levels of serum phosphate within the normal range may also be associated with adverse outcomes. We performed a post hoc analysis of data from the Cholesterol And Recurrent Events (CARE) study. Baseline serum phosphate levels were measured in 4127 fasting participants who were randomized to receive pravastatin 40 mg daily or placebo and followed up for a median of 59.7 months. We used Cox proportional-hazards models to examine the association between serum phosphate and adverse clinical outcomes after adjustment for potential confounders. During nearly 60 months of follow-up, 375 participants died. A significant association was noted between baseline serum phosphate level and the age-, race-, and sex-adjusted risk of all-cause death (hazard ratio per 1 mg/dL, 1.27; 95% confidence interval, 1.02 to 1.58). After categorization based on baseline phosphate level ( or =4 mg/dL) and further adjustment, a graded independent relation between phosphate and death was observed (P for trend=0.03). For instance, participants with serum phosphate > or =3.5 mg/dL had an adjusted hazard ratio for death of 1.27 (95% confidence interval, 1.02 to 1.59) compared with those with serum phosphate of <3.5 mg/dL. Higher levels of serum phosphate were also associated with increased risk of new heart failure, myocardial infarction, and the composite of coronary death or nonfatal myocardial infarction, but not the risk of stroke. We found a graded independent relation between higher levels of serum phosphate and the risk of death and cardiovascular events in people with prior myocardial infarction, most of whom had serum phosphate levels within the normal range. Given the ready availability and low cost of serum phosphate assays, this finding may prove clinically useful.
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            Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism.

            Inorganic phosphate is essential for ECM mineralization and also as a constituent of important molecules in cellular metabolism. Investigations of several hypophosphatemic diseases indicated that a hormone-like molecule probably regulates serum phosphate concentration. FGF23 has recently been recognized as playing important pathophysiological roles in several hypophosphatemic diseases. We present here the evidence that FGF23 is a physiological regulator of serum phosphate and 1,25-dihydroxyvitamin D (1,25[OH]2D) by generating FGF23-null mice. Disruption of the Fgf23 gene did not result in embryonic lethality, although homozygous mice showed severe growth retardation with abnormal bone phenotype and markedly short life span. The Fgf23(-/-) mice displayed significantly high serum phosphate with increased renal phosphate reabsorption. They also showed an elevation in serum 1,25(OH)2D that was due to the enhanced expression of renal 25-hydroxyvitamin D-1alpha-hydroxylase (1alpha-OHase) from 10 days of age. These phenotypes could not be explained by currently known regulators of mineral homeostasis, indicating that FGF23 is essential for normal phosphate and vitamin D metabolism.
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              Vegetarian compared with meat dietary protein source and phosphorus homeostasis in chronic kidney disease.

              Patients with advanced chronic kidney disease (CKD) are in positive phosphorus balance, but phosphorus levels are maintained in the normal range through phosphaturia induced by increases in fibroblast growth factor-23 (FGF23) and parathyroid hormone (PTH). This provides the rationale for recommendations to restrict dietary phosphate intake to 800 mg/d. However, the protein source of the phosphate may also be important. We conducted a crossover trial in nine patients with a mean estimated GFR of 32 ml/min to directly compare vegetarian and meat diets with equivalent nutrients prepared by clinical research staff. During the last 24 hours of each 7-day diet period, subjects were hospitalized in a research center and urine and blood were frequently monitored. The results indicated that 1 week of a vegetarian diet led to lower serum phosphorus levels and decreased FGF23 levels. The inpatient stay demonstrated similar diurnal variation for blood phosphorus, calcium, PTH, and urine fractional excretion of phosphorus but significant differences between the vegetarian and meat diets. Finally, the 24-hour fractional excretion of phosphorus was highly correlated to a 2-hour fasting urine collection for the vegetarian diet but not the meat diet. In summary, this study demonstrates that the source of protein has a significant effect on phosphorus homeostasis in patients with CKD. Therefore, dietary counseling of patients with CKD must include information on not only the amount of phosphate but also the source of protein from which the phosphate derives.
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                Author and article information

                Contributors
                Journal
                Saudi Pharm J
                Saudi Pharm J
                Saudi Pharmaceutical Journal : SPJ
                Elsevier
                1319-0164
                2213-7475
                12 January 2015
                July 2016
                12 January 2015
                : 24
                : 4
                : 494-505
                Affiliations
                [a ]Department of Clinical Pharmacy, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia
                [b ]School of Pharmacy and Medical Sciences, University of South Australia, South Australia, Australia
                Author notes
                [* ]Corresponding author at: Department of Clinical Pharmacy, College of Pharmacy, King Saud University, P.O. Box 2457, Riyadh 11451, Saudi Arabia. Shaman@ 123456ksu.edu.sa
                Article
                S1319-0164(15)00010-9
                10.1016/j.jsps.2015.01.009
                4908098
                27330380
                © 2015 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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