skip to main content

Hypomagnesaemia Refractory Hypocalcaemia PPI Mechanism — ESENeph MCQ

Instant feedback + full explanation. One question, done properly.

ModerateElectrolyte DisordersHypomagnesaemia Refractory Hypocalcaemia PPI MechanismESENeph

A 55-year-old man with CKD G3b (eGFR 35 mL/min/1.73m2) presents with tetany and positive Chvostek and Trousseau signs. Bloods: corrected calcium 1.65 mmol/L, phosphate 2.0 mmol/L, magnesium 0.4 mmol/L, PTH 2.5 pmol/L (inappropriately low). 25-OH vitamin D 70 nmol/L. He takes a PPI daily. What is the MOST important initial step in management?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: DIntravenous magnesium sulphate replacement

Severe hypomagnesaemia (<0.5 mmol/L) causes hypocalcaemia through TWO mechanisms: (1) impaired PTH secretion (magnesium is required for PTH exocytosis from parathyroid cells — hence the inappropriately low PTH) and (2) skeletal resistance to PTH action. Calcium replacement alone will be ineffective until magnesium is corrected, because PTH secretion cannot respond to the calcium signal without adequate magnesium. The priority is IV magnesium sulphate (8 mmol over 20 minutes followed by infusion). PPI-induced hypomagnesaemia is an increasingly recognised cause — PPIs impair intestinal magnesium absorption via TRPM6 channel inhibition. Calcium will be given simultaneously for symptomatic tetany but will not persist without magnesium correction.

Reference: https://guidelines.ukkidney.org