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Phosphate (Phosphorus) 

  • Author: Alina G Sofronescu, PhD; Chief Editor: Eric B Staros, MD  more...
 
Updated: Mar 16, 2015
 

Reference Range

Phosphate concentration is characterized by a high physiological variation, depending on age, gender, physiological state (eg, pregnancy), and even season (due to the seasonal variation of vitamin D which is directly involved in the regulation of phosphate concentration).

Therefore, separate reference intervals have been established according to the age and gender:[1, 2, 3, 4, 5]

In males, the reference range is as follows:

  • Age 0-12 months - Not established
  • Age 1-4 years - 4.3-5.4 mg/dL
  • Age 5-13 years - 3.7-5.4 mg/dL
  • Age 14-15 years - 3.5-5.3 mg/dL
  • Age 16-17 years - 3.1-4.7 mg/dL
  • Age 18 years or older - 2.5-4.5 mg/dL

In females, the reference range is as follows:

  • Age 0-12 months - Not established
  • Age 1-7 years - 4.3-5.4 mg/dL
  • Age 8-13 years - 4-5.2 mg/dL
  • Age 14-15 years - 3.5-4.9 mg/dL
  • Age 16-17 years - 3.1-4.7 mg/dL
  • Age 18 years or older - 2.5-4.5 mg/dL
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Interpretation

Different levels of phosphate depletion may be interpreted as follows:

  • Serum phosphate 1.5-2.4 mg/dL - May be considered a moderate decrease and typically does not give rise to clinical signs and symptoms
  • Serum phosphate lower than 1.5 mg/dL - May lead to muscle weakness, red cell hemolysis, or coma, as well as bone deformity and impaired bone growth
  • Serum phosphate lower than 1 mg/dL - Considered critical and may be life-threatening

Among inpatients, hypophosphatemia is relatively frequent.

When rapid elevations of serum phosphate levels are documented, the most urgent associated problem is typically hypocalcemia with tetany, seizures, and hypotension. (See Hyperphosphatemia.) Another long-term effect of such elevations is soft-tissue calcification.

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Collection and Panels

Preferred specimen

Preferred specimens are as follows:

  • Plasma, serum
  • Urine specimens (24 h timed collection)

Acceptable containers/tubes

Acceptable containers are as follows:

  • Green top tube (sodium heparin, ammonium heparin, lithium heparin)
  • Red top tube (clot activator)
  • Serum separator tube
  • Plasma separator tube
  • Urine containers (may contain 6 mol/L HCl, 20-23 mL in 24 h urine collection, to prevent precipitation of phosphate complexes)

Specimen volume

Specimen volumes are as follows:

  • 0.5 mL plasma or serum (0.25 mL minimum volume)
  • 0.5 mL whole blood
  • Entire urine collection

Specimen stability

Phosphate concentration in plasma and serum will increased in unseparated specimens stored at room temperature for longer time. The specimen should be assessed promptly. If the specimen cannot be analyzed within 1 hour, the specimens should be centrifuge and the serum or plasma should be removed from the cells within 2 hours of collection.

Samples can be refrigerate at 2-8o C up to 7 days. If assays are not completed within 48 hours, or the separated sample is to be stored beyond 48 hours, samples should be frozen at -15°C to -20°C. Frozen samples should be thawed only once. Analyte deterioration may occur in samples that are repeatedly frozen and thawed.

Collection consideration and sources of pre-analytical errors

As phosphates concentration is higher inside RBC, hemolysis will lead to increase in phosphates plasma/serum concentration. Phosphate concentration increases by 4-5 mg/dl per day in hemolyzed samples stored at 4°C or RT. Grounds for specimen rejection: Gross hemolysis (hemolysis index [HI] >2).

Prolonged storage at RT and delay testing/separation lead to hydrolysis of phosphate esters (eg, glucose phosphate, creatinine phosphate) and overestimation of phosphate concentration.

Increased concentration of lipids and/or bilirubin (lipemic and icteric specimens) can interfere with accurate laboratory results.

Phosphate concentration has significant diurnal fluctuations, with peak concentration in the afternoon and evening; morning specimen collection is recommended.

Phosphate concentration, especially in urine, varies with diet, food intake and exercise; fasting serum specimens and 24 h urine collection (not random) are preferred.[1]

Measurement of phosphate

The most common assay for phosphate determination in clinical laboratories is based on a spectrophotometric method of complexing the serum inorganic phosphate with ammonium molibdate at low pH and formation of an absorbent phosphomolibdate complex that is measured by the spectrophotometer instrument.[1]

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Background

Phosphate is often referred as “phosphorus,” a practice that is inaccurate and misleading. The elemental phosphorus is only present as part of organic and inorganic compounds, and it is not present in a “free” form in the human body. Phosphorus, in the form of mono- and divalent phosphates (H2 PO4 - and HPO42-), is part of multiple compounds in the human body, such as ATP/ADP molecules, creatine phosphate, DNA/ARN, NADP/HADPH, and phospholipids.

Similarly to calcium, the phosphates are predominantly present in an inorganic form (hydroxyapatite) in our skeleton (85%). Only about 15% is present as organic compounds in our soft tissue and circulation (10% as serum proteins-bound phosphates, 35% complexed with Ca, Mag, Na, and 55% as organically bound phosphoric acid, free mono- and divalent phosphates). The ratio of mono- and divalent phosphates in circulation depend on the pH and patient status (alkalosis or acidosis), reflecting the fact the mono- and divalent phosphates function as minor buffers in plasma, but very important intracellular buffers.

Clinical laboratories are routinely measure the organically bound phosphoric acid present in circulation.[1]

Indications/applications

Quantification of phosphate levels is useful for diagnosis and management of bone, parathyroid, and renal disease, as well as various other disorders.

Hypophosphatemia

Serum phosphate concentrations below the reference interval for the appropriate age and gender reflect a hypophosphatemia status.

Among inpatients, hypophosphatemia is relatively frequent. Hypophosphatemia may result from any of the following:

Different levels of phosphate depletion may be interpreted as follows:

  • Serum phosphate 1.5-2.4 mg/dL - May be considered a moderate decrease and typically does not give rise to clinical signs and symptoms
  • Serum phosphate lower than 1.5 mg/dL - May lead to muscle weakness, red cell hemolysis, or coma, as well as bone deformity and impaired bone growth
  • Serum phosphate lower than 1 mg/dL - Considered critical and may be life-threatening

Hyperphosphatemia

Serum phosphate concentrations above the reference interval for the appropriate age and gender reflect a hyperphosphatemia status.

When rapid elevations of serum phosphate levels are documented, the most urgent associated problem is typically hypocalcemia with tetany, seizures, and hypotension. Another long-term effect of such elevations is soft-tissue calcification.

Hyperphosphatemia may result from any of the following:

Urinary phosphate

Approximately 80% of filter phosphorous is reabsorbed by renal proximal tubule cells. The regulation of urinary phosphorous excretion is principally dependent on regulation of proximal tubule phosphorous reabsorption. Urinary phosphate varies with age, gender, muscle mass, renal function, diet, and few other factors. Therefore, normalization of measure phosphate concentration to creatinine concentration allows calculation of renal phosphate threshold and renal phosphate clearance: UPO4 (24 h collection)/GFR. This index reflects better the renal phosphate reabsorption and excretion.[1]

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Contributor Information and Disclosures
Author

Alina G Sofronescu, PhD Assistant Professor, Board Certified Clinical Chemist, Technical Director of Clinical Chemistry Laboratory, Department of Pathology and Microbiology, University of Nebraska Medical Center

Alina G Sofronescu, PhD is a member of the following medical societies: American Association for Clinical Chemistry, Canadian Society of Clinical Chemists

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

References
  1. Tietz Textbook of Clinical Chemistry, Edited by Burtis and Ashwood. Philadelphia, PA: WB Saunders Co; 1994.

  2. Yu GC, Lee DB. Clinical disorders of phosphorus metabolism. West J Med. 1987 Nov. 147(5):569-76. [Medline].

  3. Trautvetter U, Neef N, Leiterer M, Kiehntopf M, Kratzsch J, Jahreis G. Effect of calcium phosphate and vitamin D3 supplementation on bone remodelling and metabolism of calcium, phosphorus, magnesium and iron. Nutr J. 2014 Jan 17. 13:6. [Medline]. [Full Text].

  4. Ziolkowska H, Okarska-Napierala M, Stelmaszczyk-Emmel A, Gorska E, Zachwieja K, Zurowska A, et al. Serum fibroblast growth factor 23 and calcium-phosphorus metabolism parameters in children with chronic kidney disease - preliminary report. Dev Period Med. 2014. 18(2):194-202. [Medline].

  5. Shi Y, Zhao Y, Liu J, Hou Y, Zhao Y. Educational Intervention for Metabolic Bone Disease in Patients With Chronic Kidney Disease: A Systematic Review and Meta-Analysis. J Ren Nutr. 2014 Sep 3. [Medline].

 
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