Renal Handling of Magnesium
Renal handling of magnesium is principally a filtration reabsorption process with a capacity to maximally conserve and reject magnesium when appropriate. Micropuncture studies in the dog, hamster and Psammomys, aided by ultramicroanalysis of tubular fluid with the electron microprobe, have recently added much to our knowledge of renal magnesium physiology. At the glomerulus, 70–80% of total plasma magnesium is freely filterable. Magnesium concentration rises above its ultrafilterable value along the proximal tubule, though there is a wide dispersion of concentration ratios. Mean end proximal tubule fluid to ultrafilterable (TF/UF) magnesium, reaches a mean of 1.5 in the dog and 1.65 in the rat when TF/P inulin values average 2.0 and 2.4, and is probably due to available proximal tubule in these two species. Net proximal magnesium reabsorption constitutes 25% of the filtered load and can be reduced by saline and magnesium infusion. Unlike other solutes including calcium, magnesium is poorly coupled to sodium in the proximal tubule which is poorly permeable to magnesium. The precise mechanisms of proximal magnesium transport remain undefined. In the descending limb, magnesium rises 3–5 fold above ultrafilterable concentration due to water removal in the renal medulla. There is evidence that during acute magnesium infusion, entry of magnesium into the lumen may occur prior to the hairpin bend. The ascending limb avidly reabsorbs some 60–70% of the filtered magnesium and mean distal TF/UF concentrations approximate 0.6. Ascending limb magnesium transport may be active or possibly passive accompanying active chloride removal. Furthermore, magnesium transport in this segment may be progressively reduced by acute magnesium infusion, non-reabsorbable anions and furosemide. Relatively little magnesium reabsorption occurs in the distal convoluted tubule and collecting duct under normal circumstances with about 10% of the filtered magnesium being excreted. However, there is some clearance and micropuncture evidence that suggests magnesium addition in the terminal segments during acute magnesium infusion. Data in the hamster which is highly sensitive to the action of parathyroid hormone (PTH) suggests that PTH increases magnesium as well as calcium reabsorption in the ascending limb, and beyond the distal tubule puncture site. This effect is mimicked by cyclic AMP infusion. Other factors that affect magnesium handling deserve detailed study by a variety of micropuncture approaches. The exact homeostatic mechanisms which regulate renal tubular magnesium reabsorption require further identification.
The kidney plays an important role in magnesium homeostasis. The regulatory mechanisms of magnesium handling by the kidney largely remains unknown. Normally 5–20% of the filtered load is excreted in the urine. This may drop to near unmeasurable levels in dietary magnesium deficit and rise to high levels in dietary magnesium surfeit or magnesium infusion. Some of the factors that alter magnesium reabsorption are listed in Table 1.
KeywordsProximal Tubule Ethacrynic Acid Distal Convoluted Tubule Renal Handling Tubular Fluid
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