Last updated: November 3, 2022

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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).

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

Causes of hyperphosphatemia [1][2][3]
↓ Renal excretion and/or ↑ renal reabsorption
↑ Intestinal absorption
Transcellular shifts

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


Consult nephrology as needed to help guide the diagnostic workup for identifying the underlying cause of hyperphosphatemia.

  • Obtain a detailed medical history.
  • Evaluate for renal failure (most common cause).
  • Obtain 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 etiology. [5]

Routine studies [2][5]

Additional studies [2][5]

Approach [1][4]

Consult nephrology for management.

Pharmacotherapy [1][4]

Pharmacotherapy is usually reserved for patients with chronic hyperphosphatemia (e.g., patients with CKD-MBD).

  1. 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
  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. Walls R, Hockberger R, Gausche-Hill M. Rosen's Emergency Medicine. Elsevier Health Sciences ; 2018
  4. 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
  5. 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
  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

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