Urinary Excretion

Magnesium homeostasis is essentially regulated by a process of filtration-reabsorption in the kidney. Urinary Mg excretion increases when Mg intake is in excess, whereas the kidney conserves Mg in the case of Mg deprivation. Usually, 1000mmol/24h of Mg is filtered and only 3 mmol/24 h is excreted in urine.

A total of 10-15% of the filtered Mg is reabsorbed in the proximal tubule by a passive process. The majority of filtered Mg (65%) is reabsorbed in the thick ascending loop of Henle. The reabsorption in this segment is mediated by a paracellular mechanism involving paracellin-1. It is also related to sodium transport by a dependence on the transepithelial potential generated by NaCl absorption. Thus, factors that impair NaCl reabsorption in the thick ascending loop of Henle, such as osmotic diuretics, loop diuretics, and extracellular fluid volume expansion, increase Mg excretion. At least 10-15% of the filtered Mg is reabsorbed in the distal tubule. The reabsorption occurs via an active transcellular mechanism and is under the control of special divalent cation-sensing receptors. Thus, elevated plasma Mg concentrations inhibit reabsorption of Mg from the distal tubule, leading to an increased magnesuria. Other active transport may also exist since some hormones (parathyroid hormone, glucagon, calcitonin, and insulin) may increase Mg reabsorption. Other factors may also influence Mg reabsorption, such as hypercalciuria or hypophosphatemia, which inhibit the tubular reabsorption of Mg. Metabolic alkalosis leads to renal Mg conservation, whereas metabolic acidosis is associated with urinary Mg wasting. Thus, the chronic low-grade metabolic acidosis in humans eating Western diets may contribute to decreased Mg status.

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