In contrast to other ions, magnesium is treated as an orphan by the body: there are no hormones that have a substantial role in regulating urinary magnesium excretion, and bone, the principal reservoir of magnesium, does not readily exchange with circulating magnesium.
The Mg ++ is often overlooked by physicians in the differential diagnosis because it is considered insignificant, but its role is crucial for cells function, first of all neurons and cardiomyocytes. A condition of hypocalcemia associated with hypokalemia, especially in the presence of chronic renal failure, should raise suspicion of a lack of Mg ++.
We report the case of an old man of 77 year with kidney transplant for 13 years, treated with cyclosporine, and sodium mycophenolate and steroid who, for about a month, accused impaired balance and walking instability, who fell accidentally down with wrist fracture.
Blood tests showed hypocalcemia and hypokalemia, and so we required dosage of serum and urinary magnesium. A significant reduction in the ion plasma concentration was seen, associated to a fraction of excretion inappropriately high in relation to the degree of hypomagnesemia.
The cause of this important renal loss is likely attributable to cyclosporine, a drug that has as a side effect the inhibition of the reabsorption of Mg ++ in the distal convoluted tubule. then, oral supplementation was started (244 mg of Mg ++ ion / day), with subsequent normalization, after a few days, not only of magnesiemia, but also in serum calcium and potassium levels, and improvement of neurological symptoms.
Hypomagnesaemia is common in patients with renal transplantation in therapy with calcineurin inhibitors ICN, due to the effects of such drugs on the TRPM6 transporter present in the kidney distal convoluted tubule. To prevent complications caused by chronic and severe depletion of magnesium in this particular population, we recommend periodic monitoring of magnesium plasma levels.
Full text of the article is available in Italian.