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To maintain sufficient Mg<jats:sup>2+<\/jats:sup>levels, (re)absorption of Mg<jats:sup>2+<\/jats:sup>in the intestine and kidney is tightly regulated. Genetic defects that disturb Mg<jats:sup>2+<\/jats:sup>uptake pathways, as well as drugs interfering with Mg<jats:sup>2+<\/jats:sup>(re)absorption cause hypomagnesemia. The aim of this review is to provide an overview of the molecular mechanisms underlying genetic and drug-induced Mg<jats:sup>2+<\/jats:sup>deficiencies. This leads to the identification of four main mechanisms that are affected by hypomagnesemia-causing mutations or drugs: luminal transient receptor potential melastatin type 6\/7-mediated Mg<jats:sup>2+<\/jats:sup>uptake, paracellular Mg<jats:sup>2+<\/jats:sup>reabsorption in the thick ascending limb of Henle's loop, structural integrity of the distal convoluted tubule and Na<jats:sup>+<\/jats:sup>-dependent Mg<jats:sup>2+<\/jats:sup>extrusion driven by the Na<jats:sup>+<\/jats:sup>\/K<jats:sup>+<\/jats:sup>-ATPase. 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