Hyperphosphatemia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Hyperphosphatemia is an electrolyte disturbance in which there is an abnormally elevated level of phosphate in the blood. Often, calcium levels are lowered (hypocalcemia) due to precipitation of phosphate with the calcium in tissues.

Causes

Causes by Organs System

Cardiovascular	No underlying causes
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Beractant, Cefepime
Ear Nose Throat	No underlying causes
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	No underlying causes
Hematologic	No underlying causes
Iatrogenic	No underlying causes
Infectious Disease	No underlying causes
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	No underlying causes
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	No underlying causes
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	No underlying causes

Causes in Alphabetical Order

List the causes of the disease in alphabetical order. You may need to list across the page, as seen here

Disease A

Disease B

Disease C

It can be caused by hypoparathyroidism due to the lack of PTH effect of inhibiting renal reabsorption of phosophate. Independent of parathyroid hormone (PTH) and serum 1,25-dihydroxyvitamin D level, fibroblast growth factor 23 (FGF23) regulates the sodium/phosphate cotransporter (NPT2a) by controlling renal expressions of key enzymes of vitamin D metabolism.^[1] Both NPT2a and NPT2c are regulated in a similar fashion by parathyroid hormone (PTH), FGF23, and dietary phosphate.^[2]

There are two rare autosomal recessive metabolic disorders characterized by hyperphosphatemia:

Hyperphosphatemic familial tumoral calcinosis (HFTC)^[3]
Hyperphosphatemia-hyperostosis syndrome (HHS)^[4].

The principal clinical features of HFTC are represented by ectopic periarticular calcifications associated with hyperphosphatemia.^[3] HFTC has been shown to result from mutations in two genes: GALNT3 and FGF23.^[5] The secretion of FGF23 requires O-glycosylation, which is selectively directed by GALNT3, to block processing of FGF23.^[6] Hyperphosphatemia-hyperostosis syndrome (HHS) is also characterized by radiological evidence of cortical hyperostosis.^[4] HHS is caused by mutations in GALNT3.^[7] HHS and HFTC may be different manifestations of the same disorder.^[7] Hyperphosphatemia is also commonly seen in chronic renal failure. This can also be caused by taking oral sodium phosphate solutions prescribed for bowel preparation for colonoscopy in children. Hyperphosphatemia can be induced by using hyperphosphate.^[8]

Diagnosis

History and Symptoms

Signs and symptoms include ectopic calcification, secondary hyperparathyroidism, and renal osteodystrophy. α-Klotho has been implicated in the renal and parathyroid response to hyperphosphatemia.^[9] In patients with end-stage renal disease (ESRD) the expression of osteopontin in vascular smooth muscle cells (VSMCs) is associated with hyperphosphatemia or azotemia.^[10]

Treatment

High phosphate levels can be avoided with phosphate binders and dietary restriction of phosphate.

References

↑ Shimada T, Hasegawa H, Yamazaki Y, Muto T, Hino R, Takeuchi Y, Fujita T, Nakahara K, Fukumoto S, Yamashita T (2004). “FGF-23 Is a Potent Regulator of Vitamin D Metabolism and Phosphate Homeostasis”. J Bone Miner Res. 19 (3): 429–35. doi:10.1359/JBMR.0301264. PMID 15040831. Unknown parameter |month= ignored (help)
↑ Bergwitz C, Roslin NM, Tieder M, Loredo-Osti JC, Bastepe M, Abu-Zahra H, Frappier D, Burkett K, Carpenter TO, Anderson D, Garabedian M, Sermet I, Fujiwara TM, Morgan K, Tenenhouse HS, Juppner H (2006). “SLC34A3 mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria predict a key role for the sodium-phosphate cotransporter NaPi-IIc in maintaining phosphate homeostasis”. Am J Hum Genet. 78 (2): 179–92. PMID 16358214. Unknown parameter |month= ignored (help)
↑ ^3.0 ^3.1 Barbieri AM, Filopanti M, Bua G, Beck-Peccoz P (2007). “Two novel nonsense mutations in GALNT3 gene are responsible for familial tumoral calcinosis”. J Hum Genet. 52 (5): 464–8. PMID 17351710.
↑ ^4.0 ^4.1 Frishberg Y, Topaz O, Bergman R, Behar D, Fisher D, Gordon D, Richard G, Sprecher E (2005). “Identification of a recurrent mutation in GALNT3 demonstrates that hyperostosis-hyperphosphatemia syndrome and familial tumoral calcinosis are allelic disorders”. J Mol Med. 83 (1): 33–8. PMID 15599692. Unknown parameter |month= ignored (help)
↑ Specktor P, Cooper JG, Indelman M, Sprecher E (2006). “Hyperphosphatemic familial tumoral calcinosis caused by a mutation in GALNT3 in a European kindred”. J Hum Genet. 51 (5): 487–90. PMID 16528452.
↑ Kato K, Jeanneau C, Tarp MA, Benet-Pagès A, Lorenz-Depiereux B, Bennett EP, Mandel U, Strom TM, Clausen H (2006). “Polypeptide GalNAc-transferase T3 and familial tumoral calcinosis. Secretion of fibroblast growth factor 23 requires O-glycosylation”. J Biol Chem. 281 (27): 18370–7. PMID 16638743. Unknown parameter |month= ignored (help)
↑ ^7.0 ^7.1 Ichikawa S, Guigonis V, Imel EA, Courouble M, Heissat S, Henley JD, Sorenson AH, Petit B, Lienhardt A, Econs MJ (2007). “Novel GALNT3 mutations causing hyperostosis-hyperphosphatemia syndrome result in low intact fibroblast growth factor 23 concentrations”. J Clin Endocrinol Metab. 92 (5): 1943–7. PMID 17311862. Unknown parameter |month= ignored (help)
↑ Lu W, Wang X, Zhao X (2007). “Study of vascular smooth muscle cell calcification induced by hyperphosphate and intervented by phosphonoformic acid”. J Nanjing Med Univ. 21 (6): 377–81. doi:10.1016/S1007-4376(07)60082-3. Unknown parameter |month= ignored (help)
↑ Brownstein CA, Adler F, Nelson-Williams C, Iijima J, Li P, Imura A, Nabeshima Y, Reyes-Mugica M, Carpenter TO, Lifton RP (2008). “A translocation causing increased α-Klotho level results in hypophosphatemic rickets and hyperparathyroidism”. Proc Natl Acad Sci U S A. 105 (9): 3455–60. doi:10.1073/pnas.0712361105. PMID 18308935. Unknown parameter |month= ignored (help)
↑ Nakamura H, Honda H, Inada Y, Kato N, Kato K, Kitazawa K, Sugisaki T (2006). “Osteopontin expression in vascular smooth muscle cells in patients with end-stage renal disease”. Ther Apher Dial. 10 (3): 273–7. PMID 16817793. Unknown parameter |month= ignored (help)

Template:WikiDoc Sources

[Shimada-1] Shimada T, Hasegawa H, Yamazaki Y, Muto T, Hino R, Takeuchi Y, Fujita T, Nakahara K, Fukumoto S, Yamashita T (2004). “FGF-23 Is a Potent Regulator of Vitamin D Metabolism and Phosphate Homeostasis”. J Bone Miner Res. 19 (3): 429–35. doi:10.1359/JBMR.0301264. PMID 15040831. Unknown parameter |month= ignored (help)

[Bergwitz-2] Bergwitz C, Roslin NM, Tieder M, Loredo-Osti JC, Bastepe M, Abu-Zahra H, Frappier D, Burkett K, Carpenter TO, Anderson D, Garabedian M, Sermet I, Fujiwara TM, Morgan K, Tenenhouse HS, Juppner H (2006). “SLC34A3 mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria predict a key role for the sodium-phosphate cotransporter NaPi-IIc in maintaining phosphate homeostasis”. Am J Hum Genet. 78 (2): 179–92. PMID 16358214. Unknown parameter |month= ignored (help)

[Barbieri-3] 3.0 ^3.1 Barbieri AM, Filopanti M, Bua G, Beck-Peccoz P (2007). “Two novel nonsense mutations in GALNT3 gene are responsible for familial tumoral calcinosis”. J Hum Genet. 52 (5): 464–8. PMID 17351710.

[Frishberg-4] 4.0 ^4.1 Frishberg Y, Topaz O, Bergman R, Behar D, Fisher D, Gordon D, Richard G, Sprecher E (2005). “Identification of a recurrent mutation in GALNT3 demonstrates that hyperostosis-hyperphosphatemia syndrome and familial tumoral calcinosis are allelic disorders”. J Mol Med. 83 (1): 33–8. PMID 15599692. Unknown parameter |month= ignored (help)

[Specktor-5] Specktor P, Cooper JG, Indelman M, Sprecher E (2006). “Hyperphosphatemic familial tumoral calcinosis caused by a mutation in GALNT3 in a European kindred”. J Hum Genet. 51 (5): 487–90. PMID 16528452.

[Kato-6] Kato K, Jeanneau C, Tarp MA, Benet-Pagès A, Lorenz-Depiereux B, Bennett EP, Mandel U, Strom TM, Clausen H (2006). “Polypeptide GalNAc-transferase T3 and familial tumoral calcinosis. Secretion of fibroblast growth factor 23 requires O-glycosylation”. J Biol Chem. 281 (27): 18370–7. PMID 16638743. Unknown parameter |month= ignored (help)

[Ichikawa-7] 7.0 ^7.1 Ichikawa S, Guigonis V, Imel EA, Courouble M, Heissat S, Henley JD, Sorenson AH, Petit B, Lienhardt A, Econs MJ (2007). “Novel GALNT3 mutations causing hyperostosis-hyperphosphatemia syndrome result in low intact fibroblast growth factor 23 concentrations”. J Clin Endocrinol Metab. 92 (5): 1943–7. PMID 17311862. Unknown parameter |month= ignored (help)

[Lu-8] Lu W, Wang X, Zhao X (2007). “Study of vascular smooth muscle cell calcification induced by hyperphosphate and intervented by phosphonoformic acid”. J Nanjing Med Univ. 21 (6): 377–81. doi:10.1016/S1007-4376(07)60082-3. Unknown parameter |month= ignored (help)

[Brownstein-9] Brownstein CA, Adler F, Nelson-Williams C, Iijima J, Li P, Imura A, Nabeshima Y, Reyes-Mugica M, Carpenter TO, Lifton RP (2008). “A translocation causing increased α-Klotho level results in hypophosphatemic rickets and hyperparathyroidism”. Proc Natl Acad Sci U S A. 105 (9): 3455–60. doi:10.1073/pnas.0712361105. PMID 18308935. Unknown parameter |month= ignored (help)

[Nakamura-10] Nakamura H, Honda H, Inada Y, Kato N, Kato K, Kitazawa K, Sugisaki T (2006). “Osteopontin expression in vascular smooth muscle cells in patients with end-stage renal disease”. Ther Apher Dial. 10 (3): 273–7. PMID 16817793. Unknown parameter |month= ignored (help)

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