ETIOLOGY Hyperphosphatemia may be due to reduced renal excretion, increased phosphate movement out of cells into the ECF, or increased phosphorus or vitamin D intake. Hyperphosphatemia is most apt to be seen with renal dysfunction. It may also be seen with hypoparathyroidism or any problem associated with hypocalcemia or hypomagnesemia.
PHYSIOLOGIC EFFECTS Problems due to hyperphosphatemia are usually those due to associated renal failure, hypocalcemia, or the hypomagnesemia that is usually present.
THERAPY Therapy is aimed at treating the underlying cause and restricting calcium phosphate intake to less than 200 mg/day. With normal renal function, phosphate excretion can be increased with saline (1 to 2 L every 4 to 6 h) and acetazolamide (500 mg every 6 h). Phosphorus absorption from the gastrointestinal tract is decreased with oral phosphate binders (i.e., aluminum carbonate or hydroxide 30 to 45 mL qid). These binders also absorb phosphate secreted into the gut lumen and are of benefit even if no oral phosphorus is given. If clinically significant hypocalcemia exists, calcium should be cautiously administered. If renal failure is present, calcium carbonate is the treatment of choice to avoid aluminum toxicity. Hemodialysis may be required.
It may take years to correct the structural changes in bone that occur secondarily to long-term hypophosphatemia.
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