Hyperphosphatemia

Source: Wikipedia, the free encyclopedia.
Not to be confused with hypophosphatemia (low phosphate levels in the blood).
Hyperphosphatemia
high blood bilirubin[1]
TreatmentDecreasing intake, calcium carbonate[1]
FrequencyUnclear[2]

Hyperphosphatemia is an

low calcium levels which can result in muscle spasms.[1]

Causes include

high blood bilirubin levels.[1]

Treatment may include eating a phosphate low diet and

normal saline or dialysis may be used.[1] How commonly it occurs is unclear.[2]

Signs and symptoms

Signs and symptoms include

chronic kidney disease-mineral and bone disorder (CKD-MBD).[3]

Causes

Impaired renal phosphate excretion[4]
Massive extracellular fluid phosphate loads[4]

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.[citation needed]

Chronic kidney failure: When the kidneys are not working well, there will be increased phosphate retention.[citation needed
]

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

Diagnosis

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.[5] It is considered significant when levels are greater than 1.6 mmol/L (5 mg/dL).[2]

Units

Phosphates in blood exist in a

millimoles per liter (mmol/L) are often used to denote the phosphate concententration. If milligrams per decililiter (mg/dL) is used, it often denotes the mass of phosphorus bound to phosphates, but not the mass of some individual phosphate.[6]

Treatment

High phosphate levels can be avoided with

phosphate binders and dietary restriction of phosphate.[5] 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.[5] Phosphate-binding medications include sevelamer, lanthanum carbonate, calcium carbonate, and calcium acetate.[7] Previously aluminum hydroxide was the medication of choice, but its use has been largely abandoned due to the increased risk of aluminum toxicity.[8]

References

  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. ^
    ISBN 978-1437711110
    .
  3. ^ "KDIGO Guideline for Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)". Archived from the original on 4 March 2017. Retrieved 7 February 2016. {{cite journal}}: Cite journal requires |journal= (help)
  4. ^ a b Longo et al., Harrison's Principles of Internal Medicine, 18th ed., p.3089
  5. ^ a b c "Hyperphosphatemia - Endocrine and Metabolic Disorders - Merck Manuals Professional Edition". Merck Manuals Professional Edition. Merck Sharp & Dohme Corp. Retrieved 23 October 2017.
  6. ISBN 9780323478717
    .
  7. OCLC 830669119.{{cite book}}: CS1 maint: others (link
    )
  8. S2CID 19833271
    .

External links

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