Definition, Etiology, PathogenesisTop
Hyperphosphatemia is defined as a serum inorganic phosphate [Pi] >1.6 mmol/L (>5 mg/dL).
1) Impaired renal Pi excretion due to acute or chronic renal failure (the most frequent cause), hypoparathyroidism, parathyroid hormone (PTH) resistance, excess growth hormone, severe hypomagnesemia, bisphosphonates, or activating mutations of the gene encoding the sodium/phosphate cotransporter type 2a or 2c.
2) Excessive Pi release from cells due to rhabdomyolysis, tumor lysis syndrome, hemolysis, severe acidosis, malignant hyperthermia, or strenuous exercise.
3) Excessive Pi intake due to milk-alkali syndrome, laxatives containing Pi, or parenteral use of Pi.
4) Excessive absorption of Pi from the gastrointestinal (GI) tract due to vitamin D overdose.
Hyperphosphatemia leads to hypocalcemia (as a result of calcium binding and calcium deposition in the soft tissues, a factor markedly accelerating the development of atherosclerosis) and inhibits the synthesis of 1,25(OH)2D3, which subsequently leads to secondary hyperparathyroidism.
No signs or symptoms are specific for hyperphosphatemia. Clinical presentation depends on the underlying condition.
The diagnosis of hyperphosphatemia is based on measurement of serum [Pi] (>1.6 mmol/L [>5 mg/dL]).
Signs and symptoms may indicate the underlying cause of hyperphosphatemia. Studies useful in establishing the cause of hyperphosphatemia include serum levels of creatinine, calcium, magnesium, PTH, and vitamin D, and urinary Pi excretion.
1. Treatment of the underlying condition is the mainstay of the management of hypophosphatemia.
2. Reduce total body phosphate content:
1) Recommend dietary restriction of high-phosphate foods (see Phosphate Disturbances).
2) Use substances that bind Pi in the lumen of the GI tract: calcium carbonate or calcium acetate 3 to 6 g/d, sevelamer 1.5 to 6 g/d, lanthanum carbonate 200 to 1200 mg/d. These drugs are to be taken usually in divided doses during or immediately before meals.
3) In patients with normal renal function and acute hyperphosphatemia, induce forced diuresis with a loop diuretic to increase renal Pi excretion.
4) In patients with end-stage kidney disease, use intensive hemodialysis (this is the only way to remove excess Pi).
3. See also management in patients with tumor lysis syndrome.