Disorders of Phosphate: Hyperphosphatemia
Hyperphosphatemia is defined as serum [Pi] > 4.5 mg/dL. Spurious increase in serum [Pi] is called pseudohyperphosphatemia . It is rather rare but has been described in conditions of hyperglobulinemia, hypertriglyceridemia, and hyperbilirubinemia. This spurious increase has been attributed to the interference of proteins and triglycerides in the colorimetric assay of phosphate. The causes of true hyperphosphatemia can be grouped under three major categories: (1) addition of phosphate from the intracellular fluid (ICF) to extracellular fluid (ECF) compartment; (2) a decrease in renal excretion of phosphate; and (3) drugs. In clinical practice, acute and chronic kidney diseases are probably the most significant causes of hyperphosphatemia.
KeywordsHyperphosphatemia Pseudohyperphosphatemia Hyperglobulinemia Hypertriglyceridemia Hyperbilirubinemia Kidney injury Sodium phosphate
- 5.Barreto DV, Barreto Fde C, de Carvalho AB, Cuppari L, Draibe SA, Dalboni MA, Moyses RM, Neves KR, Jorgetti V, Miname M, Santos RD, Canziani ME. Phosphate binder impact on bone remodeling and coronary calcification–results from the BRiC study. Nephron Clin Pract. 2008;110:273–83.CrossRefGoogle Scholar
- 6.Qunibi W, Moustafa M, Muenz LR, et al. A 1-year randomized trial of calcium acetate versus sevelamer on progression of coronary artery calcification in hemodialysis patients with comparable lipid control: The calcium acetate renagel evaluation-2 (CARE-2) Study. Am J Kidney Dis. 2008;51:952–65.PubMedCrossRefGoogle Scholar
- 9.St Peter WL, Liu J, Weinhandl E, Fan Q. A comparison of sevelamer and calcium-based phosphate binders on mortality, hospitalization, and morbidity in hemodialysis: a secondary analysis of the dialysis clinical outcomes revisited (DCOR) randomized trial using claims data. Am J Kidney Dis. 2008;51:445–54.PubMedCrossRefGoogle Scholar
- 12.Kuro-O M. Phosphate and KLOTHO. Kidney Int. 2011;79(suppl 121):S20–3.Google Scholar
- 10.Hruska KA, Levi M, Slatopolsky E. Disorders of phosphorus, calcium, and magnesium metabolism. In: Coffman TM, Falk RJ, Molitoris BA et al, Editors. Schrier’s diseases of the kidney. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2013. pp. 2116–81.Google Scholar