Abstract
Hypophosphatemia is defined as a serum phosphorus level below the age-appropriate normal range. Acute hypophosphatemia is most commonly seen in the setting of a critical illness, whereas chronic hypophosphatemia is more likely to be of endocrine origin. The most common endocrine etiologies of chronic hypophosphatemia include vitamin D deficiency, hyperparathyroidism, and inherited forms of hypophosphatemic rickets mediated by excess fibroblast growth factor 23. Phosphate homeostasis, mechanisms of hypophosphatemia, and pertinent aspects of evaluation and management are discussed in this chapter.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
Amanzadeh J, Reilly RF Jr. Hypophosphatemia: an evidence-based approach to its clinical consequences and management. Nat Clin Pract Nephrol. 2006;2(3):136–48.
Sharma S, Hashmi MF, Castro D. Hypophosphatemia. In: StatPearls. Treasure Island, FL: StatPearls Publishing LLC; 2019.
Kleinman K, McDaniel L, Molloy M, editors. The Harriet Lane Handbook: The Johns Hopkins Hospital, 22nd Edition. Elsevier; 2020. p. 974.
Takeda E, Taketani Y, Sawada N, Sato T, Yamamoto H. The regulation and function of phosphate in the human body. BioFactors (Oxford, England). 2004;21(1–4):345–55.
Bergwitz C, Juppner H. Phosphate sensing. Adv Chronic Kidney Dis. 2011;18(2):132–44.
Blaine J, Chonchol M, Levi M. Renal control of calcium, phosphate, and magnesium homeostasis. Clin J Am Soc Nephrol. 2015;10(7):1257–72.
White KE, Larsson TE, Econs MJ. The roles of specific genes implicated as circulating factors involved in normal and disordered phosphate homeostasis: frizzled related protein-4, matrix extracellular phosphoglycoprotein, and fibroblast growth factor 23. Endocr Rev. 2006;27(3):221–41.
Clinkenbeard EL, White KE. Systemic control of bone homeostasis by FGF23 signaling. Curr Mol Biol Rep. 2016;2(1):62–71.
Kurnik BR, Hruska KA. Mechanism of stimulation of renal phosphate transport by 1,25-dihydroxycholecalciferol. Biochim Biophys Acta. 1985;817(1):42–50.
Root AW, FBDJ MD. Disorders of mineral homeostasis in children and adolescents. In: Sperling MA, editor. Pediatric endocrinology. 4th ed. Philadelphia, PA: Elsevier; 2014. p. 734–845.
Creo AL, Epp LM, Buchholtz JA, Tebben PJ. Prevalence of metabolic bone disease in tube-fed children receiving elemental formula. Horm Res Paediatr. 2018;90(5):291–8.
Leitner M, Burstein B, Agostino H. Prophylactic phosphate supplementation for the inpatient treatment of restrictive eating disorders. J Adolesc Health. 2016;58(6):616–20.
Bustos Lozano G, Hidalgo Romero A, Melgar Bonis A, Ureta Velasco N, Orbea Gallardo C, Pallas Alonso C. [Early hypophosphataemia in at risk newborns. Frequency and magnitude]. Anales De Pediatria (Barcelona, Spain : 2003). 2018;88(4):216–22.
Lotz M, Zisman E, Bartter FC. Evidence for a phosphorus-depletion syndrome in man. N Engl J Med. 1968;278(8):409–15.
Pivnick EK, Kerr NC, Kaufman RA, Jones DP, Chesney RW. Rickets secondary to phosphate depletion. A sequela of antacid use in infancy. Clin Pediatr. 1995;34(2):73–8.
Shields HM. Rapid fall of serum phosphorus secondary to antacid therapy. Gastroenterology. 1978;75(6):1137–41.
Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ (Clinical research ed). 2008;336(7659):1495–8.
Carpenter TO, Imel EA, Holm IA, Jan de Beur SM, Insogna KL. A clinician's guide to X-linked hypophosphatemia. J Bone Miner Res. 2011;26(7):1381–8.
Assadi F. Hypophosphatemia: an evidence-based problem-solving approach to clinical cases. Iran J Kidney Dis. 2010;4(3):195–201.
Yoshimatsu S, Hossain MI, Islam MM, Chisti MJ, Okada M, Kamoda T, et al. Hypophosphatemia among severely malnourished children with sepsis in Bangladesh. Pediatr Int. 2013;55(1):79–84.
Shah SK, Shah L, Bhattarai S, Giri M. Rhabdomyolysis due to severe hypophosphatemia in diabetic ketoacidosis. JNMA. 2015;53(198):137–40.
Choi HS, Kwon A, Chae HW, Suh J, Kim DH, Kim HS. Respiratory failure in a diabetic ketoacidosis patient with severe hypophosphatemia. Ann Pediatr Endocrinol Metabol. 2018;23(2):103–6.
de Oliveira Iglesias SB, Pons Leite H, de Carvalho WB. Hypophosphatemia-induced seizure in a child with diabetic ketoacidosis. Pediatr Emerg Care. 2009;25(12):859–61.
Pajak A, Krolak-Olejnik B, Szafranska A. Early hypophosphatemia in very low birth weight preterm infants. Adv Clin Exp Med. 2018;27(6):841–7.
Gonzalez Ballesteros LF, Ma NS, Gordon RJ, Ward L, Backeljauw P, Wasserman H, et al. Unexpected widespread hypophosphatemia and bone disease associated with elemental formula use in infants and children. Bone. 2017;97:287–92.
Uday S, Sakka S, Davies JH, Randell T, Arya V, Brain C, et al. Elemental formula associated hypophosphataemic rickets. Clin Nutr (Edinburgh, Scotland). 2019;38(5):2246–50.
Walton RJ, Bijvoet OL. Nomogram for derivation of renal threshold phosphate concentration. Lancet (London, England). 1975;2(7929):309–10.
Yoshida T, Yoshida N, Monkawa T, Hayashi M, Saruta T. Dietary phosphorus deprivation induces 25-hydroxyvitamin D(3) 1alpha-hydroxylase gene expression. Endocrinology. 2001;142(5):1720–6.
Imel EA, Econs MJ. Approach to the hypophosphatemic patient. J Clin Endocrinol Metab. 2012;97(3):696–706.
Carpenter TO. The expanding family of hypophosphatemic syndromes. J Bone Miner Metab. 2012;30(1):1–9.
Gohil A, Imel EA. FGF23 and associated disorders of phosphate wasting. Pediatr Endocrinol Rev. 2019;17(1):17–34.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2021 Springer Nature Switzerland AG
About this chapter
Cite this chapter
Robinson, C. (2021). Hypophosphatemia. In: Stanley, T., Misra, M. (eds) Endocrine Conditions in Pediatrics. Springer, Cham. https://doi.org/10.1007/978-3-030-52215-5_7
Download citation
DOI: https://doi.org/10.1007/978-3-030-52215-5_7
Published:
Publisher Name: Springer, Cham
Print ISBN: 978-3-030-52214-8
Online ISBN: 978-3-030-52215-5
eBook Packages: MedicineMedicine (R0)