Magnesium: The Forgotten Electrolyte That Runs the Others

The master key: why magnesium runs the others

Magnesium is a cofactor for hundreds of enzymes and, crucially, for the pumps and channels that set the other ions. Every molecule of ATP the body uses is really Mg-ATP: magnesium is the ion that makes cellular energy work, which is why a deficit ripples so widely. Two consequences dominate the clinic. First, magnesium restrains renal potassium loss — it normally blocks a potassium channel (ROMK) in the distal nephron that leaks potassium into the urine. When magnesium falls, that brake is released and the kidney wastes potassium relentlessly. No amount of intravenous potassium keeps up, because it flows straight out again. This is the mechanism behind refractory hypokalaemia — a rule threaded through the whole Hypokalaemia chapter. Second, magnesium is required for the parathyroid gland to secrete PTH and for the tissues to respond to it; a low magnesium blunts PTH, so calcium falls too and resists replacement. One under-measured cation is therefore quietly setting both potassium and calcium.

Hypomagnesaemia: the common, important one

Low magnesium comes from three routes: you lose it from the gut, you lose it from the kidney, or you never take it in. Gastrointestinal loss is the classic route: prolonged diarrhoea, malabsorption, and — a genuinely important drug cause students forget — long-term proton-pump inhibitors (omeprazole and its relatives), which impair intestinal magnesium absorption and are now a recognised cause of chronic hypomagnesaemia, cross-linking straight to the Gastrointestinal section. Renal loss is the other great source: loop diuretics (furosemide) and thiazides both increase urinary magnesium; alcohol and chronic alcoholism cause direct renal wasting (and go hand-in-hand with poor intake); and a roll-call of nephrotoxic drugs strips magnesium through the tubule — aminoglycosides (gentamicin), amphotericin B, cisplatin, and the calcineurin inhibitors (ciclosporin, tacrolimus). Finally, poor intake and refeeding: the starved or alcoholic patient starts depleted, and when feeding restarts the insulin surge drives magnesium into cells — one of the electrolytes that crashes in refeeding syndrome, alongside phosphate and potassium.

What low magnesium looks like

Clinically, hypomagnesaemia mimics low calcium — and no wonder, since it often causes it. The dominant theme is neuromuscular excitability: tremor, muscle twitching, tetany, and in severe cases seizures. The membranes of nerve and muscle become unstable and fire too easily. The other danger is cardiac: magnesium stabilises the myocardium, and a deficit predisposes to arrhythmias — most famously a role in torsades de pointes, the polymorphic ventricular tachycardia that complicates a prolonged QT interval. This is a direct bridge to the Cardiovascular section, and it carries a treatment fact worth memorising: intravenous magnesium is the treatment for torsades de pointes regardless of the serum magnesium level, because it stabilises the ventricular membrane in the acute event. Because the blood level poorly reflects total-body stores, a normal serum magnesium does not exclude deficiency — treat the patient in front of you, especially the alcoholic or the refractory hypokalaemia.

Replacement is chosen by severity and by how sick the patient is. For mild or chronic deficiency, oral magnesium salts (magnesium glycerophosphate or magnesium oxide) are used — but their dose is capped by an unavoidable side effect: unabsorbed magnesium is an osmotic laxative, so pushing the dose causes diarrhoea (the very reason magnesium salts are sold as laxatives). For severe, symptomatic, or arrhythmic hypomagnesaemia, give intravenous magnesium sulfate; it is the definitive treatment when the patient is seizing, tetanic, or in torsades. And always remember the coupling: when you replace magnesium, recheck and replace the potassium and calcium it was dragging down.

Hypermagnesaemia: rare, and almost always iatrogenic

High magnesium is far less common, because healthy kidneys excrete an excess with ease. It takes two things together: a kidney that can't clear it (renal failure) plus a magnesium load. The load is usually a drug — magnesium-containing antacids or laxatives given to a patient with poor renal function — or, importantly, therapeutic magnesium infused deliberately, most classically in obstetrics for the treatment of pre-eclampsia and eclampsia, cross-linking to the Obstetrics chapter. The features unfold as a descending, orderly loss of function as the level climbs: first the deep tendon reflexes disappear (an early, checkable warning sign), then respiratory depression, then hypotension and bradycardia, and finally cardiac arrest. Because reflexes go early, they are the bedside monitor during any magnesium infusion — losing them is the signal to stop.

The antidote is the ion magnesium spends its life antagonising: calcium. Management begins with the obvious — stop all magnesium — then support the circulation with fluids and promote excretion with a loop diuretic if kidney function allows, or dialysis in renal failure. But the specific antidote is intravenous calcium gluconate, which directly antagonises magnesium at the neuromuscular junction and the heart, buying time by reversing the paralysis and cardiac depression while magnesium is cleared. This is exactly the same calcium-versus-magnesium antagonism you meet in the treatment of magnesium toxicity during eclampsia therapy — a shared fact across the Obstetrics and Toxicology chapters. Magnesium and calcium are physiological rivals at the membrane, and here you deploy one to undo an overdose of the other.