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. [2]
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:
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Intracellular shift of phosphate (eg, post-insulin administration, respiratory alkalosis, hyperalimentation, glucose administration)
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Lower renal phosphate threshold or renal phosphate wasting (secondary parathyroidism, renal tubular damage, Fanconi syndrome, familial hypophosphatemia)
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Loss of phosphate from the gastrointestinal (GI) tract (vomiting, diarrhea, phosphate binding antacids, malabsorption syndrome)
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Primary hyperparathyroidism
Different levels of phosphate depletion may be interpreted as follows:
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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
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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
See AlsoVitamin D and Kidney Damage -
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:
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Decreased renal phosphate excretion (eg, reduced GFR, renal failure, acute kidney disease, chronic kidney disease)
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Increased renal tubular resorption
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Increased phosphate intake (eg, phosphate-containing laxatives or enemas)
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Extracellular shift of phosphate
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Loss of phosphate from intracellular stores (diabetic ketoacidosis/ketoacidosis or lactic acidosis)
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Cell lysis (eg, rhabdomyolisis, intravascular hemolysis, leukemia, lymphoma, cytotoxic therapy)
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. [2]
