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For further information, see CMDT Part 21-11: Hyperphosphatemia

Key Features

Essentials of Diagnosis

  • Advanced chronic kidney disease (CKD) is the most common cause

  • Hyperphosphatemia in the presence of hypercalcemia imposes a high risk of metastatic calcification

General Considerations

  • The two most common etiologies of hyperphosphatemia are decreased kidney clearance from CKD and transcellular shift

  • Increased dietary intake of phosphates in the setting of advanced CKD can cause hyperphosphatemia

  • Phosphate containing laxatives taken as preparation for a gastrointestinal procedure routinely cause transient hyperphosphatemia, unless the patient has impaired kidney function

  • Rapid cell breakdown from tumor lysis syndrome, rhabdomyolysis and massive hemolysis, releases intracellular phosphate

  • Hyperphosphatemia from insulin deficiency can occur in diabetic ketoacidosis

  • These patients, however, are typically phosphate depleted and are at risk for developing hypophosphatemia with insulin therapy


  • Massive load of phosphate into the extracellular fluid

    • Exogenous sources

      • Hypervitaminosis D

      • Laxatives or enemas containing phosphate

      • Intravenous phosphate supplement

    • Endogenous sources

      • Rhabdomyolysis (especially if chronic kidney disease coexists)

      • Tumor lysis by chemotherapy, particularly lymphoproliferative diseases

      • Metabolic acidosis (lactic acidosis, ketoacidosis)

      • Respiratory acidosis (phosphate incorporation into cells is disturbed)

  • Decreased excretion into urine

    • Chronic kidney disease

    • Acute kidney injury

    • Hypoparathyroidism

    • Pseudohypoparathyroidism

    • Acromegaly

  • Pseudohyperphosphatemia

    • Plasma cell myeloma

    • Hyperbilirubinemia

    • Hypertriglyceridemia

    • Hemolysis in vitro

Clinical Findings

  • The clinical manifestations are those of the underlying disorder or associated condition

  • Acute hyperphosphatemia is generally asymptomatic and symptoms are generally associated with concurrent hypocalcemia


  • In addition to elevated phosphate, blood chemistry abnormalities are those of the underlying disease


  • Treatment is directed at the underlying cause

  • Intravenous calcium

    • Can be given in life-threatening cases of acute hyperphosphatemia with symptomatic hypocalcemia and ECG changes (QTc prolongation)

    • Should be avoided in asymptomatic patients due to the risk of vascular calcification

  • Hemodialysis may be necessary in patients with impaired kidney function

  • Oral phosphate binders

    • Used in chronic hyperphosphatemia to decrease dietary phosphate intake and reduce absorption

    • Examples include

      • Calcium acetate

      • Calcium carbonate

      • Sevelamer

      • Ferric citrate


When to Admit

  • Patients with acute severe hyperphosphatemia require hospitalization for emergent therapy, possibly including dialysis

  • Concomitant illnesses, such as acute kidney injury or cell lysis, may necessitate admission


Criscuolo  M  et al. Tumor lysis syndrome: review of pathogenesis, risk factors and management of a medical emergency. Expert Rev Hematol. 2016;9:197.
[PubMed: 26629730]  
Ketteler  M  et al. Treating hyperphosphatemia—current and advancing drugs. Expert Opin Pharmacother. 2016;17:1873.
[PubMed: 27643443]  
Palmer  SC  et al. Phosphate-binding agents in adults with CKD: a network meta-analysis of randomized trials. Am J Kidney Dis. 2016;68:691.
[PubMed: 27461851]  

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