Editing Hyperphosphatemia

{{Short description|Excess phosphate in the blood}}
{{cs1 config|name-list-style=vanc}}
{{distinguish|text=[[hypophosphatemia]] (low phosphate levels in the blood)}}
{{Infobox medical condition (new)
| name            = Hyperphosphatemia
| synonyms        =
| image           = Phosphate Group.svg
| caption         = Phosphate group chemical structure
| pronounce       =
| field           = [[Endocrinology]], [[nephrology]]
| symptoms        = None, calcium deposits, muscle spasms<ref name=Mer2018/>
| complications   = [[Low blood calcium]]<ref name=Mer2018/>
| onset           =
| duration        =
| types           =
| causes          = [[Kidney failure]], [[pseudohypoparathyroidism]], [[hypoparathyroidism]], [[diabetic ketoacidosis]], [[tumor lysis syndrome]], [[rhabdomyolysis]]<ref name=Mer2018/>
| risks           =
| diagnosis       = Blood phosphate > 1.46&nbsp;mmol/L (4.5&nbsp;mg/dL)<ref name=Mer2018/>
| differential    = [[dyslipidemia|High blood lipids]], [[hyperproteinemia|high blood protein]], [[hyperbilirubinemia|high blood bilirubin]]<ref name=Mer2018/>
| prevention      =
| treatment       = Decreasing intake, [[calcium carbonate]]<ref name=Mer2018/>
| medication      =
| prognosis       =
| frequency       = Unclear<ref name=Ron2008/>
| deaths          =
}}
<!-- Definition and symptoms -->
'''Hyperphosphatemia''' is an [[electrolyte disorder]] in which there is an elevated level of [[phosphate]] in the [[blood]].<ref name=Mer2018/> Most people have no symptoms while others develop [[ectopic calcification|calcium deposits]] in the soft tissue.<ref name=Mer2018/> The disorder is often accompanied by [[low calcium]] blood levels, which can result in muscle spasms.<ref name=Mer2018>{{cite web |title=Hyperphosphatemia |url=https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/electrolyte-disorders/hyperphosphatemia |website=Merck Manuals Professional Edition |access-date=27 October 2018}}</ref>

<!-- Cause and diagnosis -->
Causes include [[kidney failure]], [[pseudohypoparathyroidism]], [[hypoparathyroidism]], [[diabetic ketoacidosis]], [[tumor lysis syndrome]], and [[rhabdomyolysis]].<ref name=Mer2018/> Diagnosis is generally based on a blood phosphate level exceeding 1.46&nbsp;mmol/L (4.5&nbsp;mg/dL).<ref name=Mer2018/>  Levels may appear falsely elevated with [[dyslipidemia|high blood lipid levels]], [[hyperproteinemia|high blood protein levels]], or [[hyperbilirubinemia|high blood bilirubin levels]].<ref name=Mer2018/>

<!-- Treatment and epidemiology -->
Treatment may include a phosphate low diet and [[antacids]] like [[calcium carbonate]] that bind phosphate.<ref name=Mer2018/> Occasionally, intravenous [[normal saline]] or [[kidney dialysis]] may be used.<ref name=Mer2018/> How commonly it occurs is unclear.<ref name=Ron2008>{{cite book |last1=Ronco |first1=Claudio |last2=Bellomo |first2=Rinaldo |last3=Kellum |first3=John A. |title=SPEC - Critical Care Nephrology Expert Consult (Book Program) Pincard |date=2008 |publisher=Elsevier Health Sciences |isbn=978-1437711110 |page=533 |url=https://books.google.com/books?id=MdgvSwnlgRgC&pg=PA533 |language=en}}</ref>

==Signs and symptoms==
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).<ref>{{Cite journal|url = http://kdigo.org/home/mineral-bone-disorder/|title = KDIGO Guideline for Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)|access-date = 7 February 2016|archive-url = https://web.archive.org/web/20170304114556/http://kdigo.org/home/mineral-bone-disorder/|archive-date = 4 March 2017|url-status = dead}}</ref>

==Causes==
{| class="wikitable"
|-
| Impaired renal phosphate excretion<ref name=Har18>Longo et al., Harrison's Principles of Internal Medicine, 18th ed., p.3089</ref> ||
* [[Renal insufficiency|Decreased kidney function]]
* [[Hypoparathyroidism|Low parathyroid hormone]]
** Developmental
** Autoimmune
** After neck surgery or radiation
** Activating mutations of the calcium-sensing receptor
* Parathyroid suppression
** Parathyroid-independent hypercalcemia
*** [[Hypervitaminosis D|Vitamin D]] or [[Hypervitaminosis A|vitamin A intoxication]]
*** [[Sarcoidosis]], other granulomatous diseases
*** Immobilization, osteolytic metastases
*** [[Milk-alkali syndrome]]
** Severe [[hypermagnesemia]] or [[hypomagnesemia]]
* [[Pseudohypoparathyroidism]]
* [[Acromegaly]]
* Tumoral calcinosis
* [[Heparin]] therapy
|-
| Massive extracellular fluid phosphate loads<ref name=Har18/> ||
* Rapid administration of exogenous phosphate (intravenous, oral, rectal)
* Extensive cellular injury or necrosis
** [[Crush injury|Crush injuries]]
** [[Rhabdomyolysis]]
** [[Hyperthermia]]
** [[Fulminant hepatitis]]
** Cytotoxic therapy
** Severe [[hemolytic anemia]]
* Transcellular phosphate shifts
** [[Metabolic acidosis]]
** [[Respiratory acidosis]]
|}
[[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|date=June 2022}}

[[Chronic kidney failure]]: When the kidneys are not working well, there will be increased phosphate retention.{{citation needed|date=June 2022}}

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&nbsp;mmol/L (4.5&nbsp;mg/dL) is indicative of hyperphosphatemia, though further tests may be needed to identify the underlying cause of the elevated phosphate levels.<ref name="Merck Manual Hyperphos">{{cite web|title=Hyperphosphatemia - Endocrine and Metabolic Disorders - Merck Manuals Professional Edition|url=http://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/electrolyte-disorders/hyperphosphatemia|website=Merck Manuals Professional Edition|publisher=Merck Sharp & Dohme Corp.|access-date=23 October 2017}}</ref> It is considered significant when levels are greater than 1.6&nbsp;mmol/L (5&nbsp;mg/dL).<ref name=Ron2008/>

===Units===
Phosphates in blood exist in a [[chemical equilibrium]] of hydrogen phosphate (HPO<sub>4</sub><sup>2–</sup>) and dihydrogen phosphate (H<sub>2</sub>PO<sub>4</sub><sup>–</sup>), which have different [[mass]]es. Phosphate (PO<sub>4</sub><sup>3–</sup>) and [[phosphoric acid]] (H<sub>3</sub>PO<sub>4</sub>) are not present in significant amounts. Thus [[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.<ref>{{Cite book|title=Nephrology secrets|vauthors=Lerma EV|year=2019|isbn=9780323478717|edition=4th|pages=532–533|publisher=Elsevier |display-authors=etal}}</ref>

==Treatment==
High phosphate levels can be avoided with [[phosphate binders]] and dietary restriction of phosphate.<ref name="Merck Manual Hyperphos" /> 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.<ref name="Merck Manual Hyperphos" /> Phosphate-binding medications include [[sevelamer]], [[lanthanum carbonate]], [[calcium carbonate]], and [[calcium acetate]].<ref>{{Cite book|title=Critical care nursing : diagnosis and management|date=2014|publisher=Elsevier/Mosby|others=Urden, Linda Diann.|isbn=978-0-323-09178-7|edition=7th|location=St. Louis, Mo.|pages=716|oclc=830669119}}</ref> Previously [[Aluminium hydroxide|aluminum hydroxide]] was the medication of choice, but its use has been largely abandoned due to the increased risk of [[Aluminium toxicity in people on dialysis|aluminum toxicity]].<ref>{{Cite journal|last1=Hutchison|first1=Alastair J.|last2=Smith|first2=Craig P.|last3=Brenchley|first3=Paul E. C.|date=October 2011|title=Pharmacology, efficacy and safety of oral phosphate binders|url=http://www.nature.com/articles/nrneph.2011.112|journal=Nature Reviews Nephrology|language=en|volume=7|issue=10|pages=578–589|doi=10.1038/nrneph.2011.112|pmid=21894188|s2cid=19833271|issn=1759-5061|url-access=subscription}}</ref>

==References==
{{reflist}}

== External links ==
{{Medical resources
|  DiseasesDB      = 20722
|  ICD10           = 
|  ICD9            = {{ICD9|275.3}}
|  ICDO            = 
|  OMIM            = 
|  MedlinePlus     = 
|  eMedicineSubj   = med
|  eMedicineTopic  = 1097
|  MeshID          = D054559
}}

{{Electrolyte abnormalities}}
{{Mineral metabolic pathology}}

[[Category:Electrolyte disturbances]]
[[Category:Wikipedia medicine articles ready to translate]]