Inherited and acquired disorders of magnesium homeostasis

Purpose of review Magnesium (Mg 2+) imbalances are frequently overlooked. Hypermagnesemia usually occurs in preeclamptic women after Mg 2+ 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 Mg 2+ homeostasis. Over the last decade, the identification of the responsible genes in rare genetic disorders has enhanced our understanding of how the kidney handles Mg 2+. The different genetic disorders and medications contributing to abnormal Mg 2+ homeostasis are reviewed. Summary As dysfunctional Mg 2+ homeostasis contributes to the development of many common human disorders, serum Mg 2+ 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 Mg 2+ reabsorption by disturbing the lumen-positive potential in the thick ascending limb or the negative membrane potential in the distal convoluted tubule.