Paeds · nephrology-urology-fluids-and-electrolytes
Calcium, magnesium and phosphate disorders
Also known as Hypocalcaemia · Hypercalcaemia · Hypomagnesaemia · Hypermagnesaemia · Hypophosphataemia · Hyperphosphataemia · Mineral and bone disorder · Disorders of divalent cations and phosphate
Fellowship guide to disorders of calcium, magnesium and phosphate in children: corrected calcium and ionised fractions, neonatal early and late hypocalcaemia, hypoparathyroidism and DiGeorge syndrome, vitamin D deficiency rickets, hypercalcaemia with immobilisation and Williams syndrome, hypomagnesaemia as the cause of refractory hypocalcaemia and hypokalaemia, refeeding hypophosphataemia, X-linked hypophosphataemic rickets with excess FGF23, tumour lysis hyperphosphataemia with hypocalcaemia, and the emergency doses of intravenous calcium gluconate and magnesium sulfate.
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Calcium, magnesium and phosphate travel together. Almost all body calcium is skeletal (less than 1 percent of total calcium is in the extracellular fluid), magnesium is predominantly intracellular, and phosphate is their structural partner in hydroxyapatite, so the small serum fraction is a tightly regulated snapshot of a much larger reservoir. [3] [8] Three hormones hold the serum in range: parathyroid hormone raises calcium by resorbing bone and reabsorbing calcium in the distal tubule while it dumps phosphate; activated vitamin D (calcitriol) increases gut absorption of all three; and fibroblast growth factor 23 lowers phosphate by forcing the kidney to excrete it and by switching off calcitriol. [9] When one mineral moves, the others follow, which is why a single abnormal value almost always disturbs its neighbours.
This page treats the three minerals as one system, then splits them by the direction of the disturbance and the mechanism that drove it. Calcium sets the urgency, because a low ionised calcium can stop the heart through a prolonged QT and obstruct the airway through laryngospasm, and a high calcium can dehydrate and destabilise. [1] Magnesium is the hidden cause, because it gates both parathyroid hormone secretion and the renal potassium channel, so a deficit silently breaks calcium and potassium homeostasis at once. [7] Phosphate is the chronic bone problem and the acute refeeding and tumour lysis problem, and its value swings with age, because growing children hold far more phosphate than adults to build skeleton. [9] [12]
Overview & Definition
The first task at the bedside is to read the calcium correctly. Total calcium is reported as a concentration bound to albumin, so hypoalbuminaemia makes a normal calcium look low. About half of extracellular calcium is bound to albumin and the other half is the ionised active form, so hypoalbuminaemia makes a normal calcium look low. Order a laboratory corrected calcium (with albumin) and an ionised calcium; the ionised fraction is the value to trust in critical illness, after massive transfusion, in alkalosis and whenever the albumin is unreliable. [1] [2]
Hypocalcaemia is a total calcium below 2.2 mmol/L or an ionised calcium below 1.0 mmol/L; symptoms typically appear with a total calcium below 1.8 mmol/L, and severe features (arrhythmia, stridor, seizures) cluster below 1.6 mmol/L. Severe hypercalcaemia with dehydration or altered consciousness is an emergency. [1] Magnesium is normally 0.7 to 1.1 mmol/L, and hypomagnesaemia is a serum magnesium below 0.7 mmol/L. Phosphate is age-dependent and must be read against the local paediatric reference range, because growing children hold more phosphate than adults to build skeleton. [8]
You have read the opening of this topic. The complete unit — every section and its primary-source references — is part of the Paediatrics Fellowship fellowship atlas.
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- [1]Zieg J; Ghose S; Raina R Electrolyte disorders related emergencies in children. BMC Nephrol, 2024.PMID 39215244
- [2]Kim GK; Siller AF; Craven M; Bansal N Neonatal Endocrine Emergencies. Adv Pediatr, 2025.PMID 40582748
- [3]Mannstadt M; Bilezikian JP; Thakker RV; Hannan FM Hypoparathyroidism. Nat Rev Dis Primers, 2017.PMID 28857066
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- [5]Munns CF; Shaw N; Kiely M; Specker BL Global Consensus Recommendations on Prevention and Management of Nutritional Rickets. J Clin Endocrinol Metab, 2016.PMID 26745253
- [6]Demay MB; Pittas AG; Bikle DD; Diab DL Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab, 2024.PMID 38828931
- [7]Tseng MH; Konrad M; Ding JJ; Lin SH Clinical and genetic approach to renal hypomagnesemia. Biomed J, 2022.PMID 34767995
- [8]Kröse JL; de Baaij JHF Magnesium biology. Nephrol Dial Transplant, 2024.PMID 38871680
- [9]Haffner D; Emma F; Eastwood DM; Biosse Duplan M Clinical practice recommendations for the diagnosis and management of X-linked hypophosphataemia. Nat Rev Nephrol, 2019.PMID 31068690
- [10]Ali DS; Carpenter TO; Imel EA; Ward LM X-Linked Hypophosphatemia Management in Children: An International Working Group Clinical Practice Guideline. J Clin Endocrinol Metab, 2025.PMID 39960858
- [11]Coiffier B; Altman A; Pui CH; Younes A Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol, 2008.PMID 18509186
- [12]O'Connor G; Nicholls D Refeeding hypophosphatemia in adolescents with anorexia nervosa: a systematic review. Nutr Clin Pract, 2013.PMID 23459608
- [13]Gupta A; Dabadghao P; Sathe A; Singh A Recalcitrant hypocalcaemia responding to teriparatide therapy: a clinical insight. BMJ Case Rep, 2025.PMID 40866089