Phosphate disturbances are thankfully neglected in CICM SAQs. Fortunately for us all, up until Question 20.1 in the first paper of 2017 the college had never asked any questions about it. It appears in the Required Reading section purely for completeness (though the author is acute aware that the pursuit of completeness may lead one to contemplate disorders of molybdenum homeostasis, etc). Oh's Manual dwells briefly on phosphate and offers two Blue Boxes to describe its behaviour (Boxes 93.8 and 93.9, p. 957-958). Of the published literature, the best summary is offered by UpToDate. A highly detailed discussion is available behind another paywall, at Springer (Albaaj et al, 2003). Of free resources, the best turned out to be the eMedicine (Medscape) article by Eleanor Lederer and Vecihi Batuman (2015).

Causes of Hyperphosphataemia

Increased intake

Acute exogenous phosphate load

  • Parenteral nutrition
  • IV supplement
  • Phosphate enema or laxative (eg. the ill-fated Fleet Phospho-Soda)

Tissue breakdown

  • Rhabdomyolysis
  • Tumour lysis syndrome
  • Intravascular haemolysis

Decreased excretion

Failure of renal excretion

  • Acute or chronic renal failure

Increase in tubular phosphate resorption

  • Hypoparathyroidism
  • Acromegaly
  • Bisphosphonates
  • Vitamin D toxicity
  • Familial tumoural calcinosis

Compartment shift


Rapid cellular content loss

  • Rhabdomyolysis
  • Tumour lysis syndrome
  • Crush injury
  • Compartment syndome

Spurious hyperphosphataemia

  • Hyperlipidaemia
  • Hyperglubulinaemia (any type of immunoglobulin)
    • Waldenstrom's macroglobulinaemia
    • Monoclonal gammopathy
    • Multiple myeloma
  • High dose liposomal amphotericin
  • Hyperbilirubinaemia
  • Haemolysis
  • Sample taken into a blood tube with heparin or alteplase
Clinical Features of Hyperphosphataemia

Neurological and neuromuscular manifestations

  • Tetany (due to hypocalcemia)
  • Confusion
  • Decreased level of consciousness

Cardiovascular manifestations

  • Hypotension
  • Atrial arrhythmias
  • Increased rate of atherosclerosis

Tissue deposition

  • Calciphylaxis
  • Cardiac tissue calcification

Biochemical changes

  • Hypocalcemia
  • Hypercalciuria
  • High anion gap metabolic acidosis
  • Increased bone resorption
  • Increased calcitriol (1,25-dihydroxyvitamin D)
  • Secondary hyperparathyroidism (raised PTH)

Renal manifestations

  • Acute phosphate nephropathy


This list of clinical features was developed with the aid of articles describing accidental severe hyperphosphataemia, such as Fine et al (1997).  The authors offer two cases of their own, as well as summarising all case reports of adults with massive hyperphosphataemia. The blood results are offered in mg/dL, which is annoying, but with the use of an online calculator the author was able to determine that of the fatal overdoses, the highest recorded serum phosphate level was 19.0 mmol/L. Of the survivors, the highest recorded phosphate level was 10.0 mmol/L, reported by Zipser et al in 1975. The 41 year old male patient had ingested a sodium phosphate laxative, and had almost died as a consequence, with hypocalcemic tetany the dominant feature of presentation. Impaired renal function was implicated in the pathogenesis in almost all cases, leading one to believe that in the presence of normal renal function it would be difficult to fatally overdose on exogenous phosphate.


Ruppe, Mary D., and Suzanne M. Jan de Beur. ". Disorders of Phosphate Homeostasis." Primer on the metabolic bone diseases and disorders of mineral metabolism (2008): 317-325.

Levi, Moshe, and Mordecai Popovtzer. "Disorders of phosphate balance." Chapter 7 in Atlases of Diseases of the Kidney 1 (1999): 7-1.

Fine, Adrian, and Joan Patterson. "Severe hyperphosphatemia following phosphate administration for bowel preparation in patients with renal failure: two cases and a review of the literature." American journal of kidney diseases 29.1 (1997): 103-105.

Zipser, R. D., M. D. Bischel, and D. E. Abrams. "Hypocalcemic tetany due to sodium phosphate ingestion in acute renal failure." Nephron 14.5 (1975): 378-381.

McConnell, Thomas H. "Fatal hypocalcemia from phosphate absorption from laxative preparation." Jama 216.1 (1971): 147-148.

Delmez, James A., and Eduardo Slatopolsky. "Hyperphosphatemia: its consequences and treatment in patients with chronic renal disease." American Journal of Kidney Diseases 19.4 (1992): 303-317.

Albaaj, Fouad, and Alastair J. Hutchison. "Hyperphosphataemia in Renal Failure." Drugs 63.6 (2003): 577-596.