Unlike most other electrolytes that are maximally absorbed in the proximal tubule, magnesium is predominantly absorbed (60-70%) in the thick ascending limb of Henle's loop (TALH). Absorption is paracellular via paracellin/claudin and is coded by the claudin genes. Mutations affecting these genes cause renal magnesium wasting and hypercalciuria.

Conditions affecting the distal convoluted tubule (DCT) ( such as Gitelman's syndrome) are typically associated with hypomagnesemia, hypocalciuria and hypercalcemia and a normal ability to concentrate the urine.

Hypercalcaemia may cause a Bartter-like Syndrome by stimulating the calcium sensing receptor on the basolateral membrane of the TALH and may have the appearance of a lasix (furosemide) effect.

However, the normal serum K, absence of metabolic alkalosis and the presence of hypercalciuria do not favour a DCT or TALH dysfunction.

I would like to know what the fractional excretion of magnesium was to help decide if the magnesium loss was renal or GIT.

Thanks Mogamat for the detailed explanation. FEMg was >4% in this patient clearly donating renal magnesium wasting. The striking feature in this case is the disturbed calcium balance that is hard to explain based on single tubular dysfunction. No apparent cause for the hypercalcemia was noted and does not seem to be PTH mediated.

Thank you Zeid. I agree that the calcium homeostasis does not fit. The relationship between magnesium and calcium is complex. But to simplify things, hypomagnesemia causes functional hypoparathyroidism by reducing PATH release. This may partially explain the normal PTH in your case. By correcting the serum magnesium, you may unmask hyperparathyroidism.

See a case attached: https://academic.oup.com/ndt/article/19/4/977/1810508

Very Interesting paper Mogamat!

Thanks for sharing.

What was the phosphate and ALP in this case?

Both were normal.