The renal handling of magnesium (Mg2+). Mg is filtered at the glomerulus, with the ultrafilterable fraction of plasma Mg entering the proximal convoluted tubule (PCT). At the end of the PCT, the Mg concentration is approximately 1.7 times the initial concentra tion of Mg and about 20% of the filtered Mg has been reabsorbed. Mg reabsorption occurs passively through paracellular pathways. Hydrated Mg has a very large radius that decreases its intercellular permeability in the PCT when compared with sodium. The smaller hydrated radius of sodium is 50% to 60% reabsorbed in the PCT. No clear evidence exists of transcellular reabsorption or secretion of Mg within the mammalian PCT. In the pars recta of the proximal straight tubule (PST), Mg reabsorption can continue to occur by way of passive forces in the concentrating kidney. In states of normal hydration, however, very little Mg reabsorption occurs in the PST. Within the thin descending limb of the loop of Henle, juxtamedullary nephrons are capable of a small amount of Mg reabsorption in a state of antidiuresis or Mg depletion. This reabsorption does not occur in superficial cortical nephrons. No data exist regarding Mg reabsorption in the thin ascending limb of the loop of Henle. No Mg reabsorption occurs in the medullary portion of the thick ascending limb of the loop of Henle; whereas nearly 65% of the filtered load is absorbed in the cortical thick ascending limb of the loop of Henle in both jux-tamedullary and superficial cortical nephrons. A small amount of Mg is absorbed in the distal convoluted tubule. Mg transport in the connecting tubule has not been well quantified. Little reabsorption occurs and no evidence exists of Mg secretion within the collecting duct. Normally, 95% of the filtered Mg is reabsorbed by the nephron. In states of Mg depletion the fractional excretion of Mg can decrease to less than 1%; whereas Mg excretion can increase in states of above-normal Mg intake, provided no evidence of renal failure exists [1,2,6-9,11,12].

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