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Subject: Phosphate, Blood
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Phosphate is used in the synthesis of phosphorylated compounds. It accompanies glucose into cells. The total body content in normal adults is approximately 700–800 g. About 80–85% of phosphate is contained in bones; the remaining 15–20% is in ICF in tissue as organic phosphates (phospholipids, nucleic acids, NADP, ATP). Only 0.1% is in the ECF as inorganic phosphate, and only this fraction of phosphorus is measured in routine clinical settings.
Normal range: see Table 16.65.
Monitoring of blood phosphate level in renal, endocrine, and GI disorders
Acute or chronic renal failure (most common cause) with decreased GFR
Most causes of hypocalcemia (except vitamin D deficiency, in which it is usually decreased)
Increased tubular reabsorption or decreased glomerular filtration of phosphate
Hypoparathyroidism (idiopathic, surgical, irradiation)
Secondary hyperparathyroidism (renal rickets)
Pseudohypoparathyroidism types I and II
Other endocrine disorders (e.g., Addison disease, acromegaly, hyperthyroidism)
Sickle cell anemia
Increased cellular release of phosphate
Neoplasms (e.g., myelogenous leukemia, lymphomas)
Excessive breakdown of tissue (e.g., chemotherapy for neoplasms, rhabdomyolysis, malignant hyperthermia, lactic acidosis, acute yellow atrophy, thyrotoxicosis)
Bone disease (e.g., healing fractures, multiple myeloma [some patients], Paget disease [some patients], osteolytic metastatic tumor in bone [some patients])
Increased phosphate load: exogenous phosphate (oral or IV) form
Phosphate enemas, laxatives or infusions
Excess vitamin D intake
IV therapy for hypophosphatemia or hypercalcemia
Milk-alkali (Burnett) syndrome (some patients)
Massive blood transfusions
Hemolysis of blood
High intestinal obstruction
Sarcoidosis (some patients)
Decreased GI absorption
Decreased dietary intake
Decreased intestinal absorption, for example, malabsorption, steatorrhea, secretory diarrhea, vomiting, vitamin D deficiency, drugs (antacids, alcohol, glucocorticoids)
Decreased renal tubular reabsorption (>100 mg/day in urine during hypophosphatemia indicates excessive renal loss)
Primary (e.g., Fanconi syndrome, rickets [vitamin D deficient or dependent or familial], idiopathic hypercalciuria)
Secondary or acquired tubular disorders (e.g., hypercalcemia, excess PTH, primary hyperparathyroidism, hypokalemia, hypomagnesemia, diuresis, glycosuria, metabolic or respiratory acidosis, metabolic alkalosis, volume expansion, acute gout, dialysis)
Intracellular shift of phosphate
Growth hormone deficiency
Acidosis (especially DKA)
Nutritional recovery syndrome (rapid refeeding after prolonged starvation)
IV administration of glucose (e.g., recovery after severe burns, hyperalimentation)
Respiratory alkalosis (e.g., gram-negative bacteremia) or metabolic
Administration of anabolic steroids, androgens, epinephrine, glucagon, insulin
Cushing syndrome (some patients)
Prolonged hypothermia (e.g., open heart surgery)
TPN with inadequate phosphate supplementation
Refeeding after prolonged starvation (e.g., anorexia nervosa)
Thyrotoxic periodic paralysis
Familial hypocalciuric hypercalcemia
Severe malnutrition, malabsorption, severe diarrhea
Often more than one mechanism is operative, usually associated with prior phosphorus depletion.
Interference may occur with serum samples from patients diagnosed as having plasma cell dyscrasias and lymphoreticular malignancies associated with abnormal Ig synthesis, such as multiple myeloma, Waldenström macroglobulinemia, and heavy chain disease.
Should be measured in fasting morning specimens because of a diurnal variation. Phosphorus has a very strong biphasic circadian rhythm. Values are lowest in the morning, peak first in the late afternoon, and peak again in the late evening. The second peak is quite elevated, and results may be outside the reference range.
Levels are influenced by dietary intake, meals, and exercise.