Sample stability:
-
24 hours at 15-25 o C
-
4 days at 2-8 o C
-
1 year at -20 o C
Units: mmol/L
|
Age Group <12 months |
1.40 - 2.50 |
|
1 - <4 years |
1.10 - 2.20 |
|
4 - <15 years |
0.90 - 2.00 |
|
15 - <18 years |
0.80 - 1.85 |
|
18 years and older |
0.75 - 1.50 |
Reference intervals were updated on 31/08/2021.
Plasma phosphate reference intervals were updated on 31/08/2021 following a review of literature, local data and paediatrician agreement (the summary document can be provided upon request). The lower limit for infants has increased from 1.00mmol/L to 1.40mmol/L. For all other age groups, the changes are minor. The new ranges have been adopted by all clinical labs in Auckland.
The increase in the lower limit for infants is largely driven by the literature findings, including the local ProVIDe RCT findings (1). This study has shown that in extremely low birth weight neonates, serum phosphate <1.40mmol/L was associated with an increased risk of mortality and severe hypophosphataemia (<0.9mmol/L) was associated with five times higher odds of severe intraventricular haemorrhage. Based on this study, local NICU teams maintain serum phosphate >1.40mmol/L in the extremely low birth weight neonates. This lower limit, which is mostly specific to ELBW neonates, is also consistent with literature findings and guidelines for normal infants (2-6).
This is a diurnal variation in plasma phosphate levels - levels can be higher in the evening. For plasma phosphate, sample is preferably taken after overnight fast.
Uncertainty of Measurement: 6%
Conversion factors:
phosphorus (mg/100 mL) x 0.323 = phosphate (mmol/L)
phosphate (mmol/L) x 3.096 = phosphorus (mg/100 mL)
Principle : Colorimetric
Reagents: Roche PHOS2 kit
Analyser: Cobas c702
Causes of low phosphate:
3 primary mechanisms - decreased GI absorption, transcellular shift and renal loss.
- Decreased absorption/ low intake
o Malnutrition, vomiting, diarrhoea
o Malabsorption, vitamin D deficiency, phosphate binding antacids containing Ca, Mg, Al
o Alcoholism
- Transcellular shift, rapid uptake into cells
o Refeeding syndrome
o Dextrose/Glucose infusion
o Insulin infusion
o Recovery phase of DKA (with Dextrose/insulin infusion)
o Acute respiratory alkalosis
o Catecholamines e.g. in acute severe illness
o 'hungry bones' - e.g. post parathyroidectomy
- Increased renal tubular loss
o Primary or secondary hyperparathyroidism
o Fanconi syndrome
o Mesenchymal tumours
o Hypophosphataemic rickets
o Medications
- Diuretics: acetazolamide, thiazides, loop diuretics
- Anti-retroviral (tenofovir, adefovir)
- Iron infusion (ferric carboxymaltose). Hypophosphataemia peaks at 2 weeks post infusion and can cause severe hypophosphataemia (<0.3 mmol/L). Ferric carboxymaltose impairs the degradation of FGF23, resulting in an elevated FGF23 which leads to reduced renal reabsorption of phosphate.
- Cisplatin, tetracyclines, aminoglycosides
Extremely low serum/plasma phosphate level (usually less than 0.3 mmol/L) can cause respiratory insufficiency, muscle weakness, rhabdomyolysis, intravascular haemolysis, seizure, myocardial depression, myopathy and haemolytic anaemia.
Causes of high phosphate
- Spurious cause: Paraproteinaemia
- Storage of unseparated blood
- Increased intake/absorption: phosphate containing laxatives, enema, vitamin D intoxication
- End Stage Renal Failure
- Cell lysis - haemolysis, tumour lysis syndrome, rhabdomyolysis
- Acidosis: DKA and lactic acidosis
-
Hypoparathyroidism
References
1. Cormack BE, Jiang Y, Harding JE, et al. Neonatal refeeding syndrome and clinical outcome in extremely low-birth-weight babies: secondary cohort analysis from the ProVIDe trial. J Parenter Enteral Nutr 2021;45(1):65-78.
2. Moltu SJ, Strommen K, Blakstad EW, et al. Enhanced feeding in very-low-birth-weight infants may cause electrolyte disturbances and septicemia--a randomized, controlled trial. Clin Nutr 2013;32(2):207-12.
3. Cubillos Celis MP, Mena Nannig P. Hypophosphatemia in preterm infants: a bimodal disorder. Rev Chil Pediatr 2018;89:10-17.
4. Abd El-Rahman Atiyyah T, Abd Elraouf ElShaarawy S, Said Al- Shal A, et al. Phosphate disturbance in critically ill children in Zagazig University pediatric intensive care unit. EJHM 2020;80:782-88.
5. da Silva JSV, Seres DS, Sabino K, et al. ASPEN Consensus Recommendations for Refeeding Syndrome. Nutr Clin Pract 2020;35(2):178-95.
6. Tate, J. R. et al. 2014. Harmonising Adult and Paediatric Reference Intervals in Australia and New Zealand: An Evidence-Based Approach for Establishing a First Panel of Chemistry Analytes. Clinical Biochemitr Reviews.
7. Imel EA and Econs MJ. Approach to the hypophosphatemic patient. J Clin Endocrinol Metab 2012; 97: 696-706.
8. Manghat P, Sodi R, Swaminathan R. Phosphate homeostasisand disorders. Ann Clin Biochem. 2014;51:631---56
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If the query concerns a specific patient please include the NHI number in your email.
If email is not a suitable option, please contact the on-call chemical pathologist via Lablink (Auckland City Hospital ext. 22000 or 09-3078995).
Individual chemical pathologists may be contacted but will not be available at all times.
After-hours : contact Lablink (Auckland City Hospital ext. 22000 or 09-3078995) or hospital operator for on duty staff after hours.
Dr Samarina Musaad (Clinical Lead) : SamarinaM@adhb.govt.nz ext. 22402
Dr Cam Kyle: CampbellK@adhb.govt.nz ext 22052
Dr Weldon Chiu: WeldonC@adhb.govt.nz ext. 23427
Dr Campbell Heron: CHeron@adhb.govt.nz ext. 23427
Dr Sakunthala Jayasinghe: Sakunthala@adhb.govt.nz ext. 23427