# Magnesium Physiology > Magnesium physiology for MBBS Physiology: body distribution, renal handling in the loop, eclampsia dosing and toxicity thresholds. - Canonical URL: https://prepelephant.com/topics/mbbs/physiology/magnesium-physiology - Exam / course: MBBS · Subject: Physiology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Magnesium Physiology", PrepElephant, https://prepelephant.com/topics/mbbs/physiology/magnesium-physiology ## Direct answer The body holds about 25 grams (roughly 1,000 mmol) of magnesium — 60 per cent in bone, nearly 39 per cent intracellular (where it is the second most abundant cation after potassium) and only about 1 per cent extracellular, with a normal serum level of 1.8-2.4 mg/dL (0.75-1.0 mmol/L). Balance is gut absorption (30-40 per cent of dietary magnesium, mainly jejunum and ileum, enhanced by vitamin D) against renal excretion, where about 60-70 per cent of filtered magnesium is reabsorbed paracellularly in the cortical thick ascending limb, driven by the lumen-positive transepithelial potential — which is why loop diuretics waste magnesium. The ion cofactors more than 300 enzymes and the sodium-potassium ATPase, so hypomagnesaemia produces refractory hypokalaemia and hypocalcaemia, while hypermagnesaemia — usually iatrogenic magnesium sulphate — abolishes deep tendon reflexes first, then respiration, then cardiac conduction, with calcium gluconate as the antidote. ## What you must remember - **Distribution:** 60 per cent bone, 39 per cent intracellular (mostly muscle and soft tissue), 1 per cent extracellular fluid; serum magnesium is a poor proxy for total-body status — a third of patients with normal levels are considered depleted by loading tests. - **Renal handling:** 10-20 per cent reabsorbed in the proximal tubule, 60-70 per cent in the cortical thick ascending limb paracellularly with the lumen-positive potential (a shared mechanism with calcium — loop diuretics lose both), 5-10 per cent distal via TRPM6, the regulated channel whose mutation causes familial hypomagnesaemia. - **Enzyme cofactor role:** magnesium complexes with ATP (Mg-ATP is the true substrate of kinases), powers sodium-potassium ATPase, and is required for glycolysis, oxidative phosphorylation, DNA transcription and protein synthesis. - **Refractory hypokalaemia rule:** low magnesium disinhibits ROMK channels, causing renal potassium wasting, and disables the Na-K ATPase — no hypokalaemia will correct until magnesium is repleted; a viva favourite. - **Hypocalcaemia link:** magnesium deficiency both impairs parathyroid hormone secretion and causes PTH resistance at bone and kidney — another doubly refractory electrolyte. - **Eclampsia protocol:** magnesium sulphate 4 g intravenous loading (over 20-30 minutes) then 1-2 g per hour, monitoring reflexes, respiration and urine output — the drug of choice for seizure prophylaxis, used across Indian institutions. - **Toxicity ladder:** with hypermagnesaemia, deep tendon reflexes disappear around 7-10 mg/dL, respiratory paralysis follows near 12-15, and cardiac arrest beyond roughly 25; calcium gluconate 10 per cent 10 mL intravenous is the immediate antagonist. ## A worked case in eclampsia management A primigravida at 34 weeks with preeclampsia develops a seizure. Magnesium sulphate 4 g is given intravenously, followed by a 1-2 g per hour infusion. The physiology of safety lies in the reflex check: magnesium blocks acetylcholine release at the neuromuscular junction (presynaptic calcium channel antagonism) and depresses neuronal excitability, so the deep tendon reflex (first function to vanish as levels climb) doubles as the bedside assay. Patellar reflexes present, respiration above 12, urine output above 25-30 mL per hour: continue. Reflexes absent: stop the infusion and draw up calcium gluconate. The same membrane logic explains the arrhythmia use: magnesium suppresses early after-depolarisations in the prolonged-QT setting, which is why intravenous magnesium is first-line in torsades de pointes even when serum magnesium is normal — a pharmacological effect at the ion-channel level, not a replacement dose. In the magnesium-depleted alcoholic arriving with tremor and hypokalaemia that resists potassium chloride, the pathway is the Na-K ATPase: replete magnesium and the potassium finally retains. ## Where students slip Students rank magnesium third behind sodium and potassium, missing that it is the second most abundant intracellular cation — the standard viva probe. The second slip is site-of-reabsorption confusion — the bulk of magnesium salvage is the thick ascending limb, not the proximal tubule (unlike sodium), and this single fact explains why furosemide depletes magnesium while a potassium-sparing approach spares it. Third, the antidote question: calcium gluconate, not more diuresis, reverses acute toxicity — magnesium's neuromuscular blockade is calcium-competitive. Finally, do not wait for serum levels to fall before treating torsades; the anti-arrhythmic effect is direct. ## Frequently asked questions ### How is body magnesium distributed? About 25 grams total — 60 per cent in bone, 39 per cent intracellular (second most abundant intracellular cation after potassium) and only 1 per cent in extracellular fluid at 1.8-2.4 mg/dL. ### Where is most filtered magnesium reabsorbed? In the cortical thick ascending limb of the loop of Henle, paracellularly, driven by the lumen-positive transepithelial potential — which is why loop diuretics and hypercalciuria waste magnesium. ### Why does hypomagnesaemia cause refractory hypokalaemia? Magnesium is the cofactor of the sodium-potassium ATPase and normally blocks ROMK efflux channels; depletion causes renal potassium wasting that no amount of potassium corrects until magnesium is repleted. ### What is the dosing and monitoring of magnesium sulphate in eclampsia? A 4 g intravenous loading dose followed by 1-2 g per hour, monitored clinically by patellar reflexes, respiratory rate above 12 per minute and urine output above 25 mL per hour, with serum levels if renal impairment exists. ### What reverses magnesium toxicity and at what signs? Intravenous 10 per cent calcium gluconate; reflex disappearance is the early warning and respiratory paralysis the emergency.