Hypomagnesemia in childhood is relatively frequently noted in the neonatal period due to maternal causes, such as decreased intake due to
vomiting, overuse of laxatives, and neonatal causes such as
intrauterine growth retardation, birth
asphyxia and exchange transfusion. A very rare cause of neonatal
magnesium deficiency is called primary hypomagnesemia caused by impaired intestinal absorption of
magnesium. Reference values of serum
magnesium in cord blood are slightly lowered. Erythrocyte
magnesium content is also lowered in cord blood and during the first month after birth. Mononuclear
magnesium content shows no differences with age. Renal
magnesium loss is diagnosed by the presence of hypomagnesemia with an inappropriately high 24-hour urinary
magnesium excretion. In isolated familial hypomagnesemia an autosomal dominant as well as an autosomal recessive mode of inheritance was found. The renal
magnesium threshold is lowered in both forms but the tubular maximum is only lowered in the dominant form. In familial hypomagnesemia-
hypokalemia (
Gitelman syndrome) the renal
magnesium threshold is lowered but the tubular maximum is in the normal range. In this syndrome, with probably an autosomal recessive mode of inheritance, the renal defect might be located in the distal nephron after the medullary part of the ascending limb of the loop of Henle. The
magnesium content of mononuclear cells and erythrocytes is in the normal and lower normal range, respectively. In the
familial hypomagnesemia-hypercalciuria syndrome, hypomagnesemia is always combined with
hyperuricemia and
nephrocalcinosis.
Myopia and
horizontal nystagmus are often present.