Lab Test: Phosphate (Blood) Level
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- Measurement of phosphate level in blood to evaluate the effects of certain disease states on phosphate levels including: abnormalities in calcium homeostatis (e.g., parathyroid disease), acute alterations of intracellular metabolic requirements (e.g., refeeding after starvation or thyrotoxicosis), cell Lysis (e.g., tumor Lysis syndrome, rhabdomyolysis), primary or secondary disorders effecting gastrointestinal phosphate absorption, inappropriate nutritional supplementation, or abnormal renal function (e.g., renal insufficiency, renal failure).
- Adults: 3 - 4.5 mg/dL (1-1.4 mmol/L)
- Child: 4.5 - 6.5 mg/dL (1.45-2.10 mmol/L)
- Newborn: 4.3 - 9.3 mg/dL (1.4-3.0 mmol/L)
- Critical Values: < 1 mg/dL
- Patients hospitalized for community acquired pneumonia
- The combination of hypophosphatemia, hypocalcemia, hypokalemia, and alkalosis in hospitalized patients with bacterial pneumonia may be a predictor of illness severity. The presence of hypophosphatemia is associated with prolonged hospitalization and increased mortality. A diagnosis of Legionnaires disease should be strongly considered in patients with hypophosphatemia, as a low phosphate level is found in 50% of these patients, however, pneumonia of other etiologies can also cause hypophosphatemia.
- Diagnosis and monitoring of tumor Lysis syndrome
- Hyperphosphatemia results from the rapid release of phosphate by fragmented tumor nuclei in quantities that exceed the excretory capacity of the kidneys; associated with an LDH level >1500 international units/L.
- Dialysis should be considered if the phosphorus level is >10 mg/dL (>3.2 mmol/L) or rising rapidly.
- Initial evaluation and monitoring of diabetic ketoacidosis
- Despite total-body phosphate depletion averaging approximately 1 mmol/kg in diabetic ketoacidosis (DKA), serum phosphate levels are often normal or increased at presentation.
- The hyperphosphatemia usually observed with DKA is primarily insulin mediated.
- Serum phosphate levels decrease with insulin therapy during treatment for DKA as phosphate re-enters the intracellular compartment.
- Phosphate levels should be obtained every 2 to 4 hours during the treatment.
- Known chronic kidney disease
- Renal failure-associated hyperphosphatemia: selected National Kidney Foundation recommendations for using serum phosphorus measurements in the prevention and management of chronic kidney disease (CKD)-related metabolic bone disease:
- Metabolic acidosis
- The effect of metabolic acidosis on phosphate levels does not appear directly related to a pH phenomenon.
- Suspected and known alcoholic ketoacidosis
- Serum phosphate is commonly depressed.
- Suspected and known hypocalcemia
- Hyperphosphatemia is a finding in renal failure, primary hypoparathryoidism, and pseudohypoparathyroidism. Hypophosphatemia is found in hypovitaminosis D, malabsorption syndromes, chronic alcohol abuse, and hyperalimentation, as well as in patients receiving loop diuretics.
- Suspected hypercalcemia
- Serum phosphorus level may be decreased in patients with hypercalcemia of malignancy. An increased serum phosphorus level with hypercalcemia may occur in hypervitaminosis D or granulomatous disease.
- Suspected hyperphosphatemia
- Hyperphosphatemia can result from exogenous phosphate overload, hypoparathyroid disease, acute cell Lysis (e.g., tumor Lysis syndrome or rhabdomyolysis), metabolic acidosis, impaired renal excretion, or increased renal phosphate resorption.
- Suspected hyperventilation
- The phosphate level can decline during hyperventilation, and remain low following the cessation. A decline in phosphate may manifest as malaise, dizziness, paresthesias, disorientation and a decrease in attention span, which are also common symptoms of hyperventilation syndrome.
- Suspected hypophosphatemia
- Hypophosphatemia can result from acute increases in intracellular energy requirements as observed in refeeding after starvation, nutritional deficiency, thyrotoxicosis, gastrointestinal absorptive impairment, hyperparathyroid disease, hypercalcemia, or phosphaturia due to impaired renal phosphate absorption. Identification of a definitive etiology requires additional testing.
- Suspected rhabdomyolysis
- Muscle necrosis may cause release of phosphates from hydrolyzed nonregenerated adenosine 5"-triphosphate (ATP) into the extracellular fluid with resultant hyperphosphatemia. Serum phosphate level correlates best with serum anion gap and inversely with bicarbonate concentration. Hypophosphatemia is seen in 40% of patients with rhabdomyolysis. Patients with levels >5 mg/dL on admission have a higher frequency of hypophosphatemia later in their hospitalization.
- Suspected sepsis
- Hypophosphatemia has been associated with septic shock and poor prognosis.
- Thermal burn
- Hypophosphatemia is common with major burns and may itself be severe. Major phosphate loss appears to be urinary with exudative losses being less important. Phosphate shifting occurs during refeeding as phosphate enters the cells with glucose.
- Phosphorus in the body is in the form of a phosphate. Most of the phosphate in the body is a part of organic compounds. Only a small part of total body phosphate is inorganic phosphate (i.e., not part of another organic compound). It is the inorganic phosphate that is measured when a "phosphate", "phosphorus", "inorganic phosphorus", or "inorganic phosphate" is requested. Most of the body's inorganic phosphorus is intracellular and combined with calcium within the skeleton; however, approximately 15% of the phosphorus exists in the blood as a phosphate salt. The inorganic phosphate (measured in this test) contributes to electrical and acid-base homeostatis.
- Phosphorus levels are determined by calcium metabolism, parathormone (parathyroid hormone [PTH]), renal excretion, and to a lesser degree, intestinal absorption. Because an inverse relationship exists between calcium and phosphors, a decrease of one mineral results in an increase in the other.
- Phosphate levels follow diurnal variation; nadir prior to noon and peak prior to midnight.
- Bone and joint panel
- Enteral/Parenteral nutritional management panel
- Parathyroid panel
- Renal panel
- Transplant panel
- Calcium, blood - should be done simultaneously with phosphate measurements.
- Recent carbohydrate ingestion, including IV glucose administration, causes decreased phosphorus levels, because phosphorus enters the cell with glucose.
- Laxatives or enemas containing sodium phosphate can increase phosphorus levels.
- Drugs that may cause increased levels include: methicillin, steroids, some diuretics (furosemide and thiazides), and vitamin D (excessive).
- Drugs that may cause decreased levels include: antacids, albuterol, anesthesia agents, estrogens, insulin, oral contraceptives, and mannitol.
- If indicated, discontinue IV fluids with glucose for several hours before the test.
- Collect 5 mL of venous blood. Avoid hemolysis. Handle the tube carefully. Hemolysis can falsely elevate the phosphate level because phosphate is an intracellular ion. Cellular lysis of red blood cells will cause the intracellular phosphate to spill into the blood.
- Use a heel stick to draw blood from infants.
- Apply pressure or a pressure dressing to the venipuncture site and assess the site for bleeding.
- Take the specimen to the laboratory immediately.
- Separate from erythrocytes within 1 hour of collection to avoid spurious results.
- Indicate on the laboratory slip the time the blood was obtained.
- Store at 4°C for several days or frozen for several months
- Explain the procedure to the patient.
- Patients should be instructed to fast (overnight) prior to test.
- Bourke E et al. Assessment of hyperphosphatemia and hypophosphatemia. Clin Lab Med 1993;13(1):183-207.
- LaGow B et al., eds. PDR Lab Advisor. A Comprehensive Point-of-Care Guide for Over 600 Lab Tests. First ed. Montvale, NJ: Thomson PDR; 2007.
- Pagana K, Pagana TJ eds. Mosby's Manual of Diagnostic and Laboratory Tests. 5th Ed. St. Louis, Missouri. 2014.
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