Practice Rational Testing

Investigating hypophosphataemia

BMJ 2014; 348 doi: https://doi.org/10.1136/bmj.g3172 (Published 28 May 2014) Cite this as: BMJ 2014;348:g3172
  1. Paul Glendenning, clinical associate professor12,
  2. Damon A Bell, associate professor12,
  3. Roderick J Clifton-Bligh, associate professor3
  1. 1School of Medicine and Pharmacology, Royal Perth Hospital, University of Western Australia, Perth, WA, Australia
  2. 2Department of Clinical Biochemistry, PathWest Laboratory Medicine, Royal Perth Hospital, Perth, WA, Australia
  3. 3Kolling Institute Royal North Shore Hospital, St Leonards, NSW, Australia
  1. Correspondence to: P Glendenning, Department of Clinical Biochemistry, PathWest Laboratory Medicine, Royal Perth Hospital, Perth, WA 6000, Australia Paul.Glendenning{at}health.wa.gov.au

This article discusses common and rare causes of hypophosphataemia, appropriate investigations, and when to refer for specialist opinion

Learning points

  • Chronic or mild hypophosphataemia is often asymptomatic or may present with non-specific symptoms; severe cases may present with myopathy, respiratory or cardiac failure, altered mentation, haemolysis, or rhabdomyolysis

  • Beware of spurious preanalytical or analytical causes of hypophosphataemia such as a non-fasting sample or paraproteinaemia

  • Useful initial tests include serum electrolytes (potassium, bicarbonate, magnesium, and calcium) to assess for renal tubular disease or extrarenal causes

  • Check ionised calcium, parathyroid hormone, and 25 hydroxyvitamin D if the cause is unknown or if musculoskeletal symptoms, hypomagnesaemia, or hypoalbuminaemia are present

  • Referral for specialist management is advised if the cause of hypophosphataemia remains uncertain, severe (<0.3 mmol/L), or symptomatic, or if there is a family history of short stature or skeletal deformities consistent with rickets

A 55 year old man with a squamous cell carcinoma of the head and neck was investigated before referral for chemotherapy. He was asymptomatic and not taking any drugs. Blood test results showed phosphate 0.7 mmol/L (reference limit 0.8-1.5) and total calcium 2.34 mmol/L (2.15-2.60).

The concentration of circulating phosphate depends on intestinal absorption, renal handling, and skeletal storage, and consequently is regulated by parathyroid hormone, vitamin D, and fibroblast growth factor 23. Internal cellular redistribution of phosphate is also important and results in hypophosphataemia under specific circumstances. The box outlines the causes of hypophosphataemia, based on the physiological regulation of phosphate metabolism.

Possible causes of hypophosphataemia

Extrarenal (common)
  • Gastrointestinal—reduced intestinal absorption; insufficient oral, enteral, or parenteral phosphate intake

  • Increased intracellular sequestration (common)—refeeding syndrome; leukaemia or lymphomas; bone matrix uptake (hungry bone syndrome); diabetic ketoacidosis; respiratory alkalosis

Renal
  • Parathyroid hormone dependent (common)—primary, secondary, or tertiary (chronic kidney disease) hyperparathyroidism

  • Fibroblast growth factor 23 dependent causes (rare)—acquired (tumour induced osteomalacia) or inherited

  • Primary renal phosphate leak—acquired (common): drugs (for …

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