Lab Testing


Phosphorus Serum

SKU: 001024


Product Description

**NOTE: All laboratory testing requires an authorizing physician in order to complete the laboratory testing.**

Causes of high phosphorus: Youth; exercise; dehydration and hypovolemia; high phosphorus content enema; acromegaly; hypoparathyroidism; pseudohypoparathyroidism; bone metastases; hypervitaminosis D; sarcoidosis; milk-alkali syndrome; liver disease, such as portal cirrhosis; catastrophic events such as cardiac resuscitation, pulmonary embolism, renal failure; diabetes mellitus with ketosis; serum artifact−sample not refrigerated; overheated, hemolyzed sample, or serum allowed to remain too long on the clot.

Although phosphate accumulation occurs as renal disease progresses, hyperphosphatemia is not a feature of early renal failure; it does not usually develop before renal function has diminished to about 25% of normal. Osteitis fibrosa in uremic subjects, from excessive bone turnover, relates to hyperphosphatasia. The role of hyperphosphatemia in promotion of such secondary hyperparathyroidism is well established. A relationship to osteomalacia in hemodialysis patients exists.

Causes of low phosphorus: (Hypophosphatemia may occur with or without phosphate depletion. Serum levels vary as much as 2.0 mg/dL during the day.)

Very severely malnourished subjects may have low phosphate levels, but even in starvation, phosphorus levels usually are normal. Antacids, diuretics, and long term steroids are among the common agents bearing a relationship to severe hypophosphatemia. Recent carbohydrate ingestion decreases phosphorus, as does intravenous glucose administration; cases of hypophosphatemia relate to I.V. carbohydrate, dialysis, hyperalimentation, prolonged intravenous administration of phosphate-free fluids, metabolic states involving glucose, potassium, and pH. Depletion of phosphate occurs in diabetic ketoacidosis. Like potassium, phosphorus returns to the cell with therapy of diabetic ketoacidosis and serum levels may diminish significantly during treatment. Osmotic diuresis induced by glycosuria in poorly controlled diabetes may lead to urinary phosphate losses with negative phosphorus balance. PO4 levels may prove useful in initiation of insulin therapy, in diabetic ketoacidosis and other situations of insulin lack; with hyperglucagonemia, corticosteroid and epinephrine use, and in respiratory alkalosis. Association of hypophosphatemia with impaired glucose metabolism is thought to reflect decreased tissue sensitivity to insulin. Alcoholism and other hepatic disorders are found very frequently among patients with low PO4. Alcoholic ketosis and alcohol withdrawal are among causes of hypophosphatemia. There is a slight decrease in serum phosphorus in the last trimester of pregnancy.

Primary hyperparathyroidism and other causes of calcium elevation, including ectopic hyperparathyroidism (pseudohyperparathyroidism).

The signs and symptoms of phosphate depletion may include neuromuscular, neuropsychiatric, gastrointestinal, skeletal, and cardiopulmonary systems. Manifestations usually are accompanied by serum levels <1.0 mg/dL.

Severe hypophosphatemia is most common in elderly patients and is often found in postoperative subjects.

Complications of hypophosphatemia: Effect on RBC 2,3-diphosphoglycerate and oxygen dissociation. Depression of myocardial function (contractibility), decreased cardiac output; respiratory failure and respiratory muscle weakness; increased incidence of sepsis, impairment of bactericidal activities. CNS consequences: polyradiculopathy, paresthesias, tremor, ataxia, weakness, slurred speech, stupor, coma, seizure; joint stiffness; myopathy; renal stones, hypercalciuria secondary to renal phosphate leak; insulin resistance, glucose intolerance. Rhabdomyolysis may complicate marked hypophosphatemia. A mortality rate of 20% is described in patients whose phosphorus concentration was 1.1−1.5 mg/dL.


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