Inherited and acquired disorders of magnesium homeostasis

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Abstract

Purpose of review

Magnesium (Mg2+) imbalances are frequently overlooked. Hypermagnesemia usually occurs in preeclamptic women after Mg2+ therapy or in end-stage renal disease patients, whereas hypomagnesemia is more common with a prevalence of up to 15% in the general population. Increasing evidence points toward a role for mild-to-moderate chronic hypomagnesemia in the pathogenesis of hypertension, type 2 diabetes mellitus, and metabolic syndrome.

Recent findings

The kidneys are the major regulator of total body Mg2+ homeostasis. Over the last decade, the identification of the responsible genes in rare genetic disorders has enhanced our understanding of how the kidney handles Mg2+. The different genetic disorders and medications contributing to abnormal Mg2+ homeostasis are reviewed.

Summary

As dysfunctional Mg2+ homeostasis contributes to the development of many common human disorders, serum Mg2+ deserves closer monitoring. Hypomagnesemic patients may be asymptomatic or may have mild symptoms. In severe hypomagnesemia, patients may present with neurological symptoms such as seizures, spasms, or cramps. Renal symptoms include nephrocalcinosis and impaired renal function. Most conditions affect tubular Mg2+ reabsorption by disturbing the lumen-positive potential in the thick ascending limb or the negative membrane potential in the distal convoluted tubule.

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