Last updated: September 11, 2023

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Summarytoggle arrow icon

Hyperphosphatemia is the abnormal elevation of serum phosphate. The majority of the body's phosphate is stored in bone, while the remainder plays a critical role in the intracellular space as part of multiple proteins and, in the form of adenosine triphosphate (ATP), as part of energy stores. Serum phosphate levels are regulated by parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), vitamin D, and calcium. The most common cause of hyperphosphatemia is chronic kidney disease (CKD). In end-stage renal disease, CKD-mineral and bone disorder (CKD-MBD) leads to dysregulation of phosphate, calcium, and PTH, resulting in secondary hyperparathyroidism. Hyperphosphatemia is often asymptomatic and diagnosed serologically. Clinical features of severe hyperphosphatemia are often related to hypocalcemia. In addition, insoluble calcium phosphate formation can lead to nephrocalcinosis and calcinosis cutis. Treatment of hyperphosphatemia centers around treating the underlying cause and may also include IV fluids, hemodialysis, and, in selected cases, pharmacotherapy (e.g., phosphate binders).

Definitiontoggle arrow icon

The following serum phosphate ranges apply to adults: [2][3]

  • Normophosphatemia: serum phosphate 2.5–4.5 mg/dL
  • Hyperphosphatemia: serum phosphate > 4.5 mg/dL
  • Severe hyperphosphatemia: serum phosphate > 6.25 mg/dL

Etiologytoggle arrow icon

The causes of hyperphosphatemia listed below have been grouped by mechanism.

Causes of hyperphosphatemia [3][4][5]
↓ Renal excretion and/or ↑ renal reabsorption
↑ Intestinal absorption
Transcellular shifts

Clinical featurestoggle arrow icon

High phosphate levels cause the formation of insoluble calcium phosphate, which can lead to hypocalcemia, nephrolithiasis, and tissue calcifications.

Diagnosticstoggle arrow icon

General principles

  • Hyperphosphatemia is often identified incidentally on laboratory studies.
  • The diagnostic evaluation focuses on identifying the underlying cause.
    • Evaluate for renal failure (most common cause).
    • Obtain a detailed medical history (e.g., family medical history and medication use).
    • Consider additional studies if renal function is normal or only mildly decreased.

If hyperphosphatemia is out of proportion to renal dysfunction, additional diagnostics should be obtained to identify the underlying cause. [2]

Routine studies [2][3]

  • Serum phosphate: to confirm hyperphosphatemia and assess severity
  • BMP: to assess renal function

Additional studies [2][3]

Treatmenttoggle arrow icon

General principles [4][6]

Consult nephrology to guide management.

Pharmacotherapy [4][8][9]

Pharmacotherapy is usually reserved for patients with chronic hyperphosphatemia (e.g., patients with CKD-MBD) if dietary changes and/or hemodialysis do not maintain normal phosphate levels.

Oral phosphate binders

Additional agents

Additional agents are used in the management of hyperparathyroidism.

Referencestoggle arrow icon

  1. Leaf DE, Wolf M. A Physiologic–Based Approach to the Evaluation of a Patient With Hyperphosphatemia. Am J Kidney Dis. 2013; 61 (2): p.330-336.doi: 10.1053/j.ajkd.2012.06.026 . | Open in Read by QxMD
  2. Koumakis E, Cormier C, Roux C, Briot K. The Causes of Hypo- and Hyperphosphatemia in Humans. Calcif Tissue Int. 2020; 108 (1): p.41-73.doi: 10.1007/s00223-020-00664-9 . | Open in Read by QxMD
  3. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical ; 2018
  4. Walls R, Hockberger R, Gausche-Hill M. Rosen's Emergency Medicine. Elsevier Health Sciences ; 2018
  5. Rastogi A, Bhatt N, Rossetti S, Beto J. Management of Hyperphosphatemia in End-Stage Renal Disease: A New Paradigm. J Ren Nutr. 2021; 31 (1): p.21-34.doi: 10.1053/j.jrn.2020.02.003 . | Open in Read by QxMD
  6. Walton RJ, Russell RG, Smith R. Changes in the renal and extrarenal handling of phosphate induced by disodium etidronate (EHDP) in man.. Clin Sci Mol Med. 1975; 49 (1): p.45-56.doi: 10.1042/cs0490045 . | Open in Read by QxMD
  7. Vervloet MG, van Ballegooijen AJ. Prevention and treatment of hyperphosphatemia in chronic kidney disease. Kidney Int. 2018; 93 (5): p.1060-1072.doi: 10.1016/j.kint.2017.11.036 . | Open in Read by QxMD
  8. Ketteler M, Block GA, Evenepoel P, et al. Executive summary of the 2017 KDIGO Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) Guideline Update: what’s changed and why it matters. Kidney Int. 2017; 92 (1): p.26-36.doi: 10.1016/j.kint.2017.04.006 . | Open in Read by QxMD
  9. $Contributor Disclosures - Hyperphosphatemia. All of the relevant financial relationships listed for the following individuals have been mitigated: Joanna Jan (medical editor, is an independent contractor for GoodRx, and is a shareholder in GoodRx, Biocept, and Rite Aid). None of the other individuals in control of the content for this article reported relevant financial relationships with ineligible companies. For details, please review our full conflict of interest (COI) policy:.

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