Skip to main content

Disorders of Phosphate: Hyperphosphatemia

  • Chapter
  • First Online:
  • 3142 Accesses

Abstract

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 (Table 22.1). In clinical practice, acute and chronic kidney diseases are probably the most significant causes of hyperphosphatemia.

This is a preview of subscription content, log in via an institution.

Buying options

Chapter
USD   29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD   64.99
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever

Tax calculation will be finalised at checkout

Purchases are for personal use only

Learn about institutional subscriptions

References

  1. Chertow GM, Burke SK, Raggi P. Treat to goal working group. Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients. Kidney Int. 2002;62:245–52.

    Article  CAS  PubMed  Google Scholar 

  2. Braun J, Asmus H-G, Holzer H, et al. Long term comparison of a calcium free phosphate binder and calcium carbonate-phosphorus metabolism and cardiovascular calcification. Clin Nephrol. 2004;62:104–15.

    Article  CAS  PubMed  Google Scholar 

  3. Block GA, Spiegel DM, Ehrlich J, et al. Effects of sevelamer and calcium on coronary artery calcification in patients new to dialysis. Kidney Int. 2005;68:1815–24.

    Article  CAS  PubMed  Google Scholar 

  4. Russo D, Miranda I, Ruocco C, et al. The progression of coronary artery calcification in predialysis patients on calcium calbonate or sevelamer. Kidney Int. 2007;72:1255–61.

    Article  CAS  PubMed  Google Scholar 

  5. Barreto DV, Barreto Fde C, de Carvalho AB, Cuppari L, Draibe SA, Dalboni MA, et al. Phosphate binder impact on bone remodeling and coronary calcification–results from the BRiC study. Nephron Clin Pract. 2008;110:273–83.

    Google 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.

    Article  CAS  PubMed  Google Scholar 

  7. Takei T, Otsubo S, Uchida K, Matsugami K, Mimuro T, Kabaya T, et al. Effects of sevelamer on the progression of vascular calcification in patients on chronic haemodialysis. Nephron Clin Pract. 2008;108:c278–83.

    Google Scholar 

  8. Molony DA, Stephens BW. Derangements in phosphate metabolism in chronic kidney diseases/endstage renal disease: therapeutic considerations. Adv Chronic Kidney Dis. 2011;18:120–31.

    Article  PubMed  Google 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.

    Article  PubMed  Google Scholar 

Suggested Reading

  1. 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. p. 2116–81.

    Google Scholar 

  2. Komaba H, Lanske B. Vitamin D and Klotho in chronic kidney disease. In: Ureňa Torres PA, et al., editors. Vitamin D in chronic kidney disease. Switzerland: Springer; 2016. p. 179–94.

    Chapter  Google Scholar 

  3. Kuro-O M. Phosphate and KLOTHO. Kidney Int. 2011;79(suppl 121):S20–3.

    Article  Google Scholar 

  4. Razzaque MS. Bone-kidney axis in systemic phosphate turnover. Arch Biochem Biophys. 2014;561:154–8.

    Article  CAS  PubMed  Google Scholar 

  5. Smogorzewski MJ, Stubbs JR, Yu ASL. Disorders of calcium, magnesium, and phosphate balance. In: Skorecki K, et al., editors. Brenner and Rector’s the kidney. 10th ed. Philadelphia: Elsevier; 2016. p. 601–35.

    Google Scholar 

  6. Tonelli M, Pannu N. Oral phosphate binders in patients with kidney failure. N Engl J Med. 2010;362:1312–24.

    Article  CAS  PubMed  Google Scholar 

  7. Gutiėrrez OM. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in kidney disease. Turner N et al. Oxford textbook of clinical nephrology. 4 Oxford. Oxford University Press; 2016. 947–56.

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

Copyright information

© 2018 Springer Science+Business Media LLC

About this chapter

Cite this chapter

Reddi, A.S. (2018). Disorders of Phosphate: Hyperphosphatemia. In: Fluid, Electrolyte and Acid-Base Disorders. Springer, Cham. https://doi.org/10.1007/978-3-319-60167-0_22

Download citation

  • DOI: https://doi.org/10.1007/978-3-319-60167-0_22

  • Published:

  • Publisher Name: Springer, Cham

  • Print ISBN: 978-3-319-60166-3

  • Online ISBN: 978-3-319-60167-0

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics