Hyperphosphatemia

Hyperphosphatemia is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

  • A serum phosphate >4.5 mg/dL defines hyperphosphatemia.
  • Hyperphosphatemia is caused by (1) transcellular shift, (2) increased intake, and most commonly, (3) decreased renal excretion. In clinical practice, renal insufficiency is usually present and serves as the major predisposing factor toward the development of hyperphosphatemia.
  • Transcellular shift occurs in rhabdomyolysis, tumor lysis syndrome, and massive hemolysis as phosphorus is released from cells into the ECF. Metabolic acidosis and hypoinsulinemia reduce phosphorus flux into cells and contribute to the hyperphosphatemia sometimes seen in DKA.
  • Increased intake leading to hyperphosphatemia usually occurs in the setting of renal insufficiency, either with dietary indiscretion in chronic kidney disease or as an iatrogenic complication. The latter can be seen when Phospho-Soda enemas (e.g., Fleet) or active vitamin D analogs are given to patients with renal insufficiency.
  • Decreased renal excretion occurs most commonly in the setting of renal failure. Occasionally, hypoparathyroidism and pseudohypoparathyroidism reduce renal phosphorus clearance as well.

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General Principles

  • A serum phosphate >4.5 mg/dL defines hyperphosphatemia.
  • Hyperphosphatemia is caused by (1) transcellular shift, (2) increased intake, and most commonly, (3) decreased renal excretion. In clinical practice, renal insufficiency is usually present and serves as the major predisposing factor toward the development of hyperphosphatemia.
  • Transcellular shift occurs in rhabdomyolysis, tumor lysis syndrome, and massive hemolysis as phosphorus is released from cells into the ECF. Metabolic acidosis and hypoinsulinemia reduce phosphorus flux into cells and contribute to the hyperphosphatemia sometimes seen in DKA.
  • Increased intake leading to hyperphosphatemia usually occurs in the setting of renal insufficiency, either with dietary indiscretion in chronic kidney disease or as an iatrogenic complication. The latter can be seen when Phospho-Soda enemas (e.g., Fleet) or active vitamin D analogs are given to patients with renal insufficiency.
  • Decreased renal excretion occurs most commonly in the setting of renal failure. Occasionally, hypoparathyroidism and pseudohypoparathyroidism reduce renal phosphorus clearance as well.

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