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Hyperphosphatemia is an electrolyte disorder in which there is an elevated level of phosphate in the blood.[1] Most people have no symptoms while others develop calcium deposits in the soft tissue.[1] Often there is also low calcium levels which can result in muscle spasms.[1]

Hyperphosphatemia
Phosphate Group.PNG
Phosphate group chemical structure
SpecialtyEndocrinology, nephrology
SymptomsNone, calcium deposits, muscle spasms[1]
ComplicationsLow blood calcium[1]
CausesKidney failure, pseudohypoparathyroidism, hypoparathyroidism, diabetic ketoacidosis, tumor lysis syndrome, rhabdomyolysis[1]
Diagnostic methodBlood phosphate > 1.46 mmol/L (4.5 mg/dL)[1]
Differential diagnosisHigh blood lipids, high blood protein, high blood bilirubin[1]
TreatmentDecreasing intake, calcium carbonate[1]
FrequencyUnclear[2]

Causes include kidney failure, pseudohypoparathyroidism, hypoparathyroidism, diabetic ketoacidosis, tumor lysis syndrome, and rhabdomyolysis.[1] Diagnosis is generally based on a blood phosphate levels of greater than 1.46 mmol/L (4.5 mg/dL).[1] When levels are greater than 4.54 mmol/L (14 mg/dL) it is deemed severe.[3] Levels may appear falsely elevated with high blood lipid levels, high blood protein levels, or high blood bilirubin levels.[1]

Treatment may include eating a phosphate low diet and antacids, like calcium carbonate, that bind phosphate.[1] Occasionally intravenous normal saline or dialysis may be used.[1] How commonly it occurs is unclear.[2]

Signs and symptomsEdit

Signs and symptoms include ectopic calcification, secondary hyperparathyroidism, and renal osteodystrophy. Abnormalities in phosphate metabolism such as hyperphosphatemia are included in the definition of the new chronic kidney disease-mineral and bone disorder (CKD-MBD).[4]

CausesEdit

Impaired renal phosphate excretion[5]
Massive extracellular fluid phosphate loads[5]

Hypoparathyroidism: In this situation, there are low levels of parathyroid hormone (PTH). PTH normally inhibits reabsorption of phosphate by the kidney. Therefore, without enough PTH there is more reabsorption of the phosphate leading to a high phosphate level in the blood.

Chronic renal failure: When the kidneys are not working well, there will be increased phosphate retention.

Drugs: hyperphosphatemia can also be caused by taking oral sodium phosphate solutions prescribed for bowel preparation for colonoscopy in children.

DiagnosisEdit

The diagnosis of hyperphosphatemia is made through measuring the concentration of phosphate in the blood. A phosphate concentration greater than 1.46 mmol/l (4.5 mg/dl) is indicative of hyperphosphatemia, though further tests may be needed to identify the underlying cause of the elevated phosphate levels.[6] It is considered severe when levels are greater than 1.6 mmol/l ( 5mg/dl).[2]

TreatmentEdit

High phosphate levels can be avoided with phosphate binders and dietary restriction of phosphate.[6] If the kidneys are operating normally, a saline diuresis can be induced to renally eliminate the excess phosphate. In extreme cases, the blood can be filtered in a process called hemodialysis, removing the excess phosphate.[6]

ReferencesEdit

  1. ^ a b c d e f g h i j k l m n "Hyperphosphatemia". Merck Manuals Professional Edition. Retrieved 27 October 2018.
  2. ^ a b c Ronco, Claudio; Bellomo, Rinaldo; Kellum, John A. (2008). SPEC - Critical Care Nephrology Expert Consult (Book Program) Pincard. Elsevier Health Sciences. p. 533. ISBN 1437711111.
  3. ^ Adams, James G. (2012). Emergency Medicine: Clinical Essentials (Expert Consult - Online and Print). Elsevier Health Sciences. p. 1416. ISBN 1455733946.
  4. ^ "KDIGO Guideline for Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)". Retrieved 7 February 2016. Cite journal requires |journal= (help)
  5. ^ a b Longo et al., Harrison's Principles of Internal Medicine, 18th ed., p.3089
  6. ^ a b c "Hyperphosphatemia - Endocrine and Metabolic Disorders - Merck Manuals Professional Edition". Merck Manuals Professional Edition. Merck Sharp & Dohme Corp. Retrieved 23 October 2017.

External linksEdit

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External resources