Clinical Information

Of the phosphorus contained in the body, 88% is localized in bone in the form of hydroxyapatite. The remainder is utilized during intermediary carbohydrate metabolism and bound to physiologically important substances such as phospholipids, nucleic acids, and adenosine triphosphate (ATP). Phosphorus exists in blood in the form of inorganic phosphate and organically bound phosphoric acid. The small amount of extracellular organic phosphorus is found exclusively in the form of phospholipids. Serum contains approximately 2.5 to 4.5 mg/dL of inorganic phosphate (the fraction measure in routine biochemical assays). Serum phosphate concentrations are dependent on dietary intake and regulation by hormones such as parathyroid hormone (PTH) and 1,25 vitamin D, and systemic acid base status and may vary widely.

Hypophosphatemia may have 4 general causes: shift of phosphate from extracellular to intracellular, renal phosphate wasting, loss from the gastrointestinal tract, and loss from intracellular stores.

Hyperphosphatemia is usually secondary to an inability of the kidneys to excrete phosphate and is common in patients with chronic kidney disease stage 4 or greater. Acute hyperphosphatemia can occur as a result of tissue breakdown such as rhabdomyolysis. Other possible contributory factors are increased intake, especially in combination with chronic kidney disease, or a shift of phosphate from tissues into the extracellular fluid.