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Phosphorus is acquired by eating phosphorus-rich foods. Phosphorus is
absorbed in the GI tract and excreted in urine and a small amount in feces. It
is converted to phosphate in the body.
Both phosphate and calcium levels are regulated by parathyroid hormone
(PTH). The amount of phosphate in the blood effects the level of calcium in the
blood. Both levels are usually measured at the same time. As the serum calcium
concentration increases, the concentration of serum phosphorus decreases and
conversely as serum phosphorus increases, serum calcium decreases. The nor-
mal range of serum phosphorus is between 2.5 mg/dL and 4.5 mg/dL.
The kidneys regulate the amount of phosphate in the blood. Abnormally high
levels of serum phosphate are usually caused by kidney malfunction.

Hyperphosphatemia

Hyperphosphatemia is the condition exhibited by a patient whose serum phos-
phate is greater than 4.5 mg/dL, which is caused by:


  • Kidney disease.

  • Underactive parathyroid glands.

  • Acromegaly.

  • Rhabdomyolysis.

  • Healing fractures.

  • Untreated diabetic ketoacidosis.

  • Certain bone diseases.

  • Excessive ingestion of phosphate-containing laxatives.

  • Excessive drinking of milk.

  • Chemotherapy for neoplastic disease.

  • Excessive intake of vitamin D.

  • Decrease in magnesium levels as in alcoholism.

  • Increased phosphate levels during the last trimester of pregnancy.


Unlike hyperkalemia and hypermagnesemia, acute hyperphosphatemia causes
few sudden problems. The major effect is to cause hypocalcemia and tetany if
serum phosphate rises too rapidly. Calcium can be deposited in the tissues in
hyperphosphatemia.
The treatment for acute hyperphosphatemia is administration of phosphate
binding salts, calcium, magnesium, and aluminum although aluminum is avoided
in renal failure.

(^178) CHAPTER 10 Fluid and Electrolyte Therapy

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