Phosphate Control in Chronic Kidney Disease: an Unresolved Issue

Antonio Bellasi¹, Luca Di Lullo², Biagio Di Iorio³ and Domenico Russo⁴

Received: May 31, 2018;   Published: June 15, 2018

DOI: 10.26717/BJSTR.2018.05.001236

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Abstract

A significant body of evidence supports the notion that higher levels of serum phosphate are associated with poor survival [1-3]. Similar outcome data have been reported in end stage renal disease (ESRD) as well as individuals with various degree of renal function impairment [1-3]. However, the lack of randomized clinical trial (RCT) and a certain degree of heterogeneity among different studies in this domain preclude the definition of what is the optimal range of serum phosphate to target in different chronic kidney disease (CKD) stages [1-3]. Phosphorus is an essential element for life. It is a key factor in energy metabolism being a fundamental constituent of adenosine triphosphate (ATP) [2]. Similarly, phosphate is a core element of deoxyribonucleic acid (DNA) as well as a cell membranes.

Keywords: Phosphate Balance; Phsophorous; Phosphate Binder; Chronic Kidney Disease; Serum Phosphate; Numerous kinases; Normophosphatemia; Phosphate Homeostasis Perturbations; Placebo; Lanthanum Carbonate; Sevelamer Carbonate; Calcium Acetate; Plasma; Hyperphosphatemic

Abbreviations: ESRD: End Stage Renal Disease; CKD: Chronic Kidney Disease; ATP: Adenosine Triphosphate; DNA: Deoxyribonucleic Acid; PTH: Parathyroid Hormone; FEP: Fraction Excretion of Phosphate; RCT: Randomized Clinical Trial; FGF: Fibroblast Growth Factor

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