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Hyperphosphatemia
Last reviewed: 04.07.2025
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Hyperphosphatemia is a serum phosphate concentration greater than 4.5 mg/dL (greater than 1.46 mmol/L). Causes include chronic renal failure, hypoparathyroidism, and metabolic or respiratory acidosis. Clinical features of hyperphosphatemia may be due to concomitant hypocalcemia and may include tetany. Diagnosis is by measuring serum phosphate levels. Treatment involves restricting phosphate intake and administering phosphate-binding antacids, which include calcium carbonate.
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Causes hyperphosphatemia
Hyperphosphatemia usually results from decreased renal excretion of PO2. Advanced renal failure (SCF <20 mL/min) reduces excretion sufficiently to increase plasma PO2 levels. Impaired renal phosphate excretion in the absence of renal failure also occurs in pseudohypoparathyroidism and hypoparathyroidism. Hyperphosphatemia also occurs with excessive oral PO2 intake and excessively frequent use of PO2-containing enemas.
Hyperphosphatemia sometimes develops as a result of a massive release of PO2 ions into the extracellular space, which exceeds the excretory capacity of the kidneys. This mechanism most often develops in diabetic ketoacidosis (despite the general decrease in PO2 content in the body), injuries, non-traumatic rhabdomyolysis, as well as in systemic infections and tumor lysis syndrome. Hyperphosphatemia also plays a major role in the development of secondary hyperparathyroidism and renal osteodystrophy in patients on dialysis. Hyperphosphatemia may be false in hyperproteinemia (multiple myeloma or Waldenstrom's macroglobulinemia), hyperlipidemia, hemolysis, hyperbilirubinemia.
Symptoms hyperphosphatemia
Most patients with hyperphosphatemia are asymptomatic, but if hypocalcemia is present, symptoms of hypocalcemia, including tetany, may occur. Soft tissue calcification is commonly seen in patients with chronic renal failure.
The diagnosis of hyperphosphatemia is based on a PO2 level greater than 4.5 mg/dL (> 1.46 mmol/L). If the etiology is not obvious (eg, rhabdomyolysis, tumor lysis syndrome, renal failure, abuse of PO2-containing laxatives), additional testing is needed to exclude hypoparathyroidism or pseudohypoparathyroidism, which is characterized by resistance of target organs to PTH. It is also necessary to exclude PO2 mismeasurement by measuring serum protein, lipids, and bilirubin.
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Treatment hyperphosphatemia
The mainstay of treatment for hyperphosphatemia in patients with renal failure is to reduce PO2 intake. It is recommended to avoid foods containing large amounts of PO2 and to take phosphate binders with meals. Because of the risk of developing osteomalacia due to aluminum accumulation, calcium carbonate and calcium acetate are recommended as antacids in patients with end-stage renal disease. Recently, the risk of developing vascular calcification due to excessive formation of Ca and PO2 binding products has been identified in patients with a condition such as hyperphosphatemia and those undergoing dialysis and taking Ca-binding agents. For this reason, dialysis patients are recommended to take the PO2 binding resin, sevelamer, at a dose of 800-2400 mg 3 times daily with meals.