The glomerular filtration of magnesium (Mg). Total serum Mg consists of ionized, complexed, and protein bound fractions, 60%, 7%, and 33% of total, respectively. The complexed Mg is bound to molecules such as citrate, oxalate, and phosphate. The ultrafil-terable Mg is the total of the ionized and complexed fractions. Normal total serum Mg is approximately 1.7 to 2.1 mg/dL (about 0.70-0.90 mmol/L) [1,2,7-9,11,12].
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].
Magnesium (Mg) reabsorption in the cortical thick ascending limb (cTAL) of the loop of Henle. Most Mg reabsorption within the nephron occurs in the cTAL owing primarily to voltage-dependent Mg flux through the intercellular tight junction. Transcellular Mg movement occurs only in response to cellular metabolic needs. The sequence of events necessary to generate the lumen-positive electrochemical gradient that drives Mg reabsorption is as follows: 1) A basolateral sodium-potassium-adenosine triphosphatase (Na+-K+-ATPase) decreases intracellular sodium, generating an inside-negative electrical potential difference; 2) Intracellular K is extruded by an electroneutral K-Cl (chloride) cotrans-porter; 3) Cl is extruded by way of conductive pathways in the basolateral membrane; 4) The apical-luminal Na-2Cl-K (furosemide-sensitive) cotransport mechanism is driven by the inside-negative potential difference and decrease in intracellular Na; 5) Potassium is recycled back into the lumen by way of an apical K conductive channel; 6) Passage of approximately 2 Na molecules for every Cl molecule is allowed by the paracellular pathway (intercellular tight junction), which is cation permselective; 7) Mg reabsorption occurs passively, by way of intercellular channels, as it moves down its electrical gradient [1,2,6,7]. (Adapted from de Rouffignac and Quamme .)
Voltage-dependent net magnesium (Mg) flux in the cortical thick ascending limb (cTAL). Within the isolated mouse cTAL, Mg flux (JMg) occurs in response to voltage-dependent mechanisms. With a relative lumen-positive transepithelial potential difference (Vt), Mg reabsorption increases (positive JMg). Mg reabsorption equals zero when no voltage-dependent difference exists, and Mg is capable of moving into the tubular lumen (negative JMg) when a lumen-negative voltage difference exists [1,16]. (From di Stefano and coworkers ).
Effect of hormones on magnesium (Mg) transport in the cortical thick ascending limb (cTAL). In the presence of arginine vasopressin (AVP), glucagon (GLU), human calcitonin (HCT), parathyroid hormone (PTH), 1,4,5-isoproteronol (ISO), and insulin (INS), increases occur in Mg reabsorption from isolated segments of mouse cTALs. These hormones have no effect on medullary TAL segments. As already has been shown in Figure 4-3, these hormones affect intracellular "second messengers" and cellular Mg movement. These hormone-induced alterations can affect the paracellular permeability of the intercellular tight junction. These changes may also affect the transepithelial voltage across the cTAL. Both of these forces favor net Mg reabsorption in the cTAL [1,2,7,8]. Asterisk—significant change from preceding period; JMg—Mg flux; C—control, absence of hormone. (Adapted from de Rouffignac and Quamme .)
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