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Paeds Topicsnephrology-urology-fluids-and-electrolytes

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.

high13 referencesUpdated 5 Sept 202626 min readSource-verified · Sept 2026

Checked against its sources on 5 Sept 2026

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Red flags

  • A neonate or child with seizures, stridor or carpopedal spasm and a low ionised calcium needs intravenous 10 percent calcium gluconate now — laryngospasm can obstruct the airway and a prolonged QT can degenerate, so do not wait for the corrected value
  • Hypocalcaemia that will not correct is hypomagnesaemia until proven otherwise — low magnesium suppresses parathyroid hormone release and disinhibits renal potassium loss, so neither calcium nor potassium will be retained until magnesium is replaced
  • A child starting chemotherapy for a high-burden lymphoma or leukaemia who develops a high phosphate with a low calcium and a high potassium has tumour lysis syndrome — give aggressive hydration and rasburicase, and expect the calcium to fall further as the phosphate peaks
  • Severe hypercalcaemia presents with dehydration, altered consciousness and arrhythmia — rehydrate with isotonic saline first, then add a loop diuretic and a bisphosphonate; never give a thiazide, which worsens hypercalcaemia
  • A malnourished child or an adolescent with anorexia nervosa who is refed too fast will drop their phosphate as insulin drives it into cells — refeeding hypophosphataemia causes respiratory failure, rhabdomyolysis and cardiac collapse, so start feeds low and replace phosphate

Life stages

neonateinfanttoddlerpreschoolschool-ageadolescentyoung-adult-transition

Care settings

ed-acutewardpicunicuoutpatientretrieval

Clinical exam formats

written-only

Board mappings

  • Corrected calcium and the ionised fraction, and why albumin matters
  • Hypomagnesaemia as the hidden cause of refractory hypocalcaemia
  • Emergency dose of intravenous calcium gluconate for symptomatic hypocalcaemia
  • Vitamin D deficiency rickets versus X-linked hypophosphataemic rickets on biochemistry
  • FGF23-mediated renal phosphate wasting and the burosumab era
  • Hypercalcaemia of immobilisation and the role of bisphosphonates
  • Neonatal hypocalcaemia: early, late, and the role of DiGeorge syndrome
  • Tumour lysis syndrome and the calcium-phosphate precipitate
  • Refeeding hypophosphataemia in the malnourished child and in anorexia nervosa
  • Short case: a neonate with stridor and seizures
  • Long case: an adolescent with X-linked hypophosphataemic rickets
  • Communication station: explaining refeeding safety to a family
  • Nephrology and metabolic: mineral and bone homeostasis
  • Investigation and emergency management of hypocalcaemia
  • Inherited hypophosphataemic rickets and tubular phosphate wasting
  • Physiology of the PTH-vitamin D-FGF23 axis and the bone-kidney-gut loop
  • Biochemistry that separates rickets phenotypes
  • Pharmacology of calcium gluconate, magnesium sulfate, phosphate salts and burosumab
  • Clinical assessment of the hypocalcaemic child and the bedside signs
  • Communication: explaining a lifelong mineral disorder to a family
  • Disorders of calcium, magnesium and phosphate: definition, causes and emergency management
  • Corrected calcium and the calcium-first, magnesium-second rule
  • Tumour lysis syndrome and refeeding hypophosphataemia
  • Patient Care: mineral emergencies and cardiac monitoring
  • Medical Knowledge: the PTH-vitamin D-FGF23 axis and renal phosphate handling
  • Systems-Based Practice: safe intravenous calcium and magnesium protocols
  • Nephrology and endocrinology: divalent cation and phosphate disorders
  • Emergency management of hypocalcaemia and hypercalcaemia in children
  • Inherited hypophosphataemias and renal phosphate wasting
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Practise this topic

  • Short-answer question1
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Target exams

RACP DWERACP DCEMRCPCH TheoryMRCPCH Clinical

Red flags

  • A neonate or child with seizures, stridor or carpopedal spasm and a low ionised calcium needs intravenous 10 percent calcium gluconate now — laryngospasm can obstruct the airway and a prolonged QT can degenerate, so do not wait for the corrected value
  • Hypocalcaemia that will not correct is hypomagnesaemia until proven otherwise — low magnesium suppresses parathyroid hormone release and disinhibits renal potassium loss, so neither calcium nor potassium will be retained until magnesium is replaced
  • A child starting chemotherapy for a high-burden lymphoma or leukaemia who develops a high phosphate with a low calcium and a high potassium has tumour lysis syndrome — give aggressive hydration and rasburicase, and expect the calcium to fall further as the phosphate peaks
  • Severe hypercalcaemia presents with dehydration, altered consciousness and arrhythmia — rehydrate with isotonic saline first, then add a loop diuretic and a bisphosphonate; never give a thiazide, which worsens hypercalcaemia
  • A malnourished child or an adolescent with anorexia nervosa who is refed too fast will drop their phosphate as insulin drives it into cells — refeeding hypophosphataemia causes respiratory failure, rhabdomyolysis and cardiac collapse, so start feeds low and replace phosphate

Life stages

neonateinfanttoddlerpreschoolschool-ageadolescentyoung-adult-transition

Care settings

ed-acutewardpicunicuoutpatientretrieval

Clinical exam formats

written-only

Board mappings

  • Corrected calcium and the ionised fraction, and why albumin matters
  • Hypomagnesaemia as the hidden cause of refractory hypocalcaemia
  • Emergency dose of intravenous calcium gluconate for symptomatic hypocalcaemia
  • Vitamin D deficiency rickets versus X-linked hypophosphataemic rickets on biochemistry
  • FGF23-mediated renal phosphate wasting and the burosumab era
  • Hypercalcaemia of immobilisation and the role of bisphosphonates
  • Neonatal hypocalcaemia: early, late, and the role of DiGeorge syndrome
  • Tumour lysis syndrome and the calcium-phosphate precipitate
  • Refeeding hypophosphataemia in the malnourished child and in anorexia nervosa
  • Short case: a neonate with stridor and seizures
  • Long case: an adolescent with X-linked hypophosphataemic rickets
  • Communication station: explaining refeeding safety to a family
  • Nephrology and metabolic: mineral and bone homeostasis
  • Investigation and emergency management of hypocalcaemia
  • Inherited hypophosphataemic rickets and tubular phosphate wasting
  • Physiology of the PTH-vitamin D-FGF23 axis and the bone-kidney-gut loop
  • Biochemistry that separates rickets phenotypes
  • Pharmacology of calcium gluconate, magnesium sulfate, phosphate salts and burosumab
  • Clinical assessment of the hypocalcaemic child and the bedside signs
  • Communication: explaining a lifelong mineral disorder to a family
  • Disorders of calcium, magnesium and phosphate: definition, causes and emergency management
  • Corrected calcium and the calcium-first, magnesium-second rule
  • Tumour lysis syndrome and refeeding hypophosphataemia
  • Patient Care: mineral emergencies and cardiac monitoring
  • Medical Knowledge: the PTH-vitamin D-FGF23 axis and renal phosphate handling
  • Systems-Based Practice: safe intravenous calcium and magnesium protocols
  • Nephrology and endocrinology: divalent cation and phosphate disorders
  • Emergency management of hypocalcaemia and hypercalcaemia in children
  • Inherited hypophosphataemias and renal phosphate wasting
Key answer

Disorders of calcium, magnesium and phosphate share one endocrine loop: parathyroid hormone, vitamin D and fibroblast growth factor 23 govern how much mineral moves between bone, gut and kidney, and the serum value reflects that traffic rather than total body stores. [1] [3] Hypocalcaemia that produces tetany, seizures or a prolonged QT needs intravenous 10 percent calcium gluconate at 0.5 mL per kilogram (about 0.1 mmol per kilogram), to a maximum of about 20 mL, slowly with cardiac monitoring, and any hypocalcaemia that will not correct is hypomagnesaemia until proven otherwise, so intravenous magnesium 0.1 to 0.2 mmol per kilogram (maximum 8 mmol) is replaced first. [2] [7] Hypercalcaemia demands saline and a loop diuretic, never a thiazide, and phosphate swings with refeeding, X-linked hypophosphataemic rickets and tumour lysis, where a rising phosphate pulls calcium down as it precipitates. [11] [12]

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]

Correct the calcium before you interpret it

Total calcium binds albumin, so in hypoalbuminaemia the reported value underestimates the active fraction. Order a laboratory corrected calcium with albumin, or measure the ionised calcium directly, which is the value that matters in sepsis, alkalosis, massive transfusion and critical illness. [1] [2]

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References13ShowHide
  1. [1]Zieg J; Ghose S; Raina R Electrolyte disorders related emergencies in children. BMC Nephrol, 2024.PMID 39215244
  2. [2]Kim GK; Siller AF; Craven M; Bansal N Neonatal Endocrine Emergencies. Adv Pediatr, 2025.PMID 40582748
  3. [3]Mannstadt M; Bilezikian JP; Thakker RV; Hannan FM Hypoparathyroidism. Nat Rev Dis Primers, 2017.PMID 28857066
  4. [4]Khan AA; Guyatt G; Ali DS; Bilezikian JP Management of Hypoparathyroidism. J Bone Miner Res, 2022.PMID 36161671
  5. [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. [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. [7]Tseng MH; Konrad M; Ding JJ; Lin SH Clinical and genetic approach to renal hypomagnesemia. Biomed J, 2022.PMID 34767995
  8. [8]Kröse JL; de Baaij JHF Magnesium biology. Nephrol Dial Transplant, 2024.PMID 38871680
  9. [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. [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. [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. [12]O'Connor G; Nicholls D Refeeding hypophosphatemia in adolescents with anorexia nervosa: a systematic review. Nutr Clin Pract, 2013.PMID 23459608
  13. [13]Gupta A; Dabadghao P; Sathe A; Singh A Recalcitrant hypocalcaemia responding to teriparatide therapy: a clinical insight. BMJ Case Rep, 2025.PMID 40866089

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