Serum
mmol/L
AGE / RANGE
neonate / 1.3 – 2.6
infant / 1.3 – 2.4
1-16Y / 0.9 – 1.8
adult / 0.8 – 1.5
Approximately 85% of total body phosphate is located in bone, 10% in skeletal muscle, and less than 1% in extracellular fluid. Most dietary phosphate comes from dairy products and meat. Dietary intake greatly exceeds the normal daily requirement. The duodenum and jejunum are the major sites of phosphate absorption. The kidneys maintain phosphate balance. About 80% of filtered phosphate is reabsorbed in the proximal tubules and10% in the distal tubules. The remaining 10% is excreted in urine. PTH concentration, extracellular fluid volume, acid base status, and dietary phosphate intake regulate phosphate reabsorption. Increased PTH concentration decreases phosphate reabsorption. Fluid volume contraction increases and fluid volume expansion decreases phosphate reabsorption.
In healthy individuals, plasma phosphate concentration displays a marked diurnal variation, being lowest in the morning and highest during the night. The intra-individual variation of plasma phosphate is 15%. If fasting samples are drawn at the same time of the day, intraindividual variation decreases to 7%. Phosphate levels are lower immediately after a meal because of insulin release. Phosphate levels are higher in summer and lower in winter due to changes in vitamin D levels. Plasma phosphate levels are high at birth and remain higher in children than adults. Levels are lower in elderly men. Prolonged bed rest causes a significant rise in phosphate concentration, that gradually decreases following mobilization. Plasma phosphate levels do not change significantly during pregnancy, but tend to be higher in lactating women. Serum phosphate levels may be higher in patients with thrombocytosis due to release of intracellular phosphate from platelets during specimen clotting.
Mild hypophosphatemia ( < 0.85mmol/L) is present in about 3% of general hospital admissions, but is much more common in patients who are acutely ill, malnourished, or in ketoacidosis. Symptomatic hypophosphatemia is usually observed when plasma phosphate levels fall below 0.35 mmol/L for several days. Severe hypophosphatemia can cause muscle weakness, bone pain, tremors, seizures, cardiomyopathy, respiratory insufficiency, hypercalcuria, and decreased platelet and granulocyte function. Hyperventilation and respiratory alkalosis are the major causes of hypophosphatemia in patients with pain, anxiety, sepsis, alcoholism, severe liver disease, salicylate toxicity, head injury, heat stroke, and mechanical ventilation. Respiratory alkalosis causes increased intracellular pH, which stimulates phosphofructokinase activity resulting in increased glycolysis and incorporation of phosphate into organic intermediates. As a consequence phosphate shifts into cells. Infusion of 5% dextrose can cause a significant decrease in plasma phosphate, due to increased insulin secretion and uptake of phosphate into cells. Life threatening hypophosphatemia may occur in malnourished patients who are rapidly administered carbohydrates. Diabetic ketoacidosis causes reduced phosphate intake because of anorexia and vomiting and increased phosphate excretion due to osmotic diuresis. Primary hyperparathyroidism can cause hypophosphatemia secondary to increased urinary excretion of phosphate. Vitamin D deficiency causes hypocalcemia, secondary hyperparathyroidism, increased urinary phosphate excretion and decreased intestinal phosphate absorption. Hepatic insufficiency contributes to hypophosphatemia by decreased 25-hydroxylation of vitamin D, leading to reduced synthesis of 1,25 dihyroxy vitamin D3 Chronic diarrhoea and steatorrhoea may reduce intestinal phosphate absorption. Antacids such as aluminum hydroxide bind phosphate in the gut and prevent phosphate absorption. Other drugs such as sucralfate contain aluminum hydroxide and have a similar effect.
The incidence of mild hyperphosphatemia in a general hospital population is about 1.5%. Acute hyperphosphatemia can lead to hypocalcemia, tetany, and hypotension. A rise in the plasma calcium x phosphate product above 70 results in soft tissue calcium deposition. Renal failure accounts for more than 90% of hyperphosphatemia cases. Plasma phosphate levels begin to rise when the GFR falls below 25% of normal. Metabolic acidosis causes hyperphosphatemia by promoting a shift of phosphate out of cells and into the extracellular fluid. Tissue hypoxia increases plasma phosphate concentration due to accelerated ATP breakdown. Rhabdomyolysis, tumor lysis syndrome, and hemolysis produce severe hyperphosphatemia because of the massive release of intracellular phosphate. Hypoparathyroidism, acromegaly, and thyrotoxicosis cause hyperphosphatemia by reducing urinary phosphate excretion. Oral or parenteral phosphate administration can cause hyperphosphatemia, especially if renal function is compromised. Enemas with a high phosphate content can cause hyperphosphatemia, hypocalcemia, and tetany.
High doses of liposomal drug formulations may cause falsely elevated results for plasma phosphorus. Some of the most commonly used liposomal formulations are;
| Amphotericin B | AmBisome |
| Cytarabine | DepoCyt |
| Doxorubicin | Doxil |
The interference has been attributed to the phospholipid bilayer in the liposomal envelope that is used to facilitate drug delivery.
Prolonged blood sample storage and in vitro hemolysis can cause artifactual hyperphosphatemia. Some patients with multiple myeloma have a spuriously high plasma phosphate concentration due to interference with the test method.
Local test
1 day
Can be added on to an existing request up to 4 days following sample receipt
Specimen Labelling Procedure
8210
