The normal fractional urinary excretion of filtered magnesium is about
5%. In magnesium deficiency in man, the kidneys can normally reduce t
he 24-hour urinary magnesium excretion to less than 1 mmol (24 mg) via
unknown mechanisms, and initially without a fall in plasma magnesium
concentration. Renal magnesium wasting may be defined as a urinary exc
retion greater than 1 mmol/day in the presence of hypomagnesemia (plas
ma magnesium < 0.7 mmol/l). Congenital renal magnesium wasting occurs
in several syndromes including Bartter's syndrome in which it is assoc
iated with hypercalciuria, and the defect may be in the thick ascendin
g limb of Henle's loop, and Gitelman's syndrome in which there is hypo
calciuria, and the defect may be in the distal convoluted tubule. Othe
r causes of renal magnesium wasting include diabetes mellitus, hyperca
lcemia and diuretics. Magnesium wasting may also result from various t
oxicities including those of cis-platinum, in which the biochemical fe
atures resemble Gitelman's syndrome, and those of aminoglycosides, pen
tamidine and cyclosporin. Calcitriol deficiency may also contribute to
renal magnesium wasting in some circumstances. Mild hypermagnesemia m
ay occur in familial hypocalciuric hypercalcemia and may reflect abnor
mal sensitivity of the loop of Henle to calcium and magnesium ions. By
contrast, the hypermagnesemia that occurs in chronic renal failure re
sults from the reduced glomerular filtration of magnesium.