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      Mechanism of Hypokalemia in Magnesium Deficiency

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      Journal of the American Society of Nephrology
      American Society of Nephrology (ASN)

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          Abstract

          Magnesium deficiency is frequently associated with hypokalemia. Concomitant magnesium deficiency aggravates hypokalemia and renders it refractory to treatment by potassium. Herein is reviewed literature suggesting that magnesium deficiency exacerbates potassium wasting by increasing distal potassium secretion. A decrease in intracellular magnesium, caused by magnesium deficiency, releases the magnesium-mediated inhibition of ROMK channels and increases potassium secretion. Magnesium deficiency alone, however, does not necessarily cause hypokalemia. An increase in distal sodium delivery or elevated aldosterone levels may be required for exacerbating potassium wasting in magnesium deficiency.

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          Most cited references10

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          Inward rectifier potassium channels.

          The past three years have seen remarkable progress in research on the molecular basis of inward rectification, with significant implications for basic understanding and pharmacological manipulation of cellular excitability. Expression cloning of the first inward rectifier K channel (Kir) genes provided the necessary break-through that has led to isolation of a family of related clones encoding channels with the essential functional properties of classical inward rectifiers, ATP-sensitive K channels, and muscarinic receptor-activated K channels. High-level expression of cloned channels led to the discovery that classical inward so-called anomalous rectification is caused by voltage-dependent block of the channel by polyamines and Mg2+ ions, and it is now clear that a similar mechanism results in inward rectification of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-kainate receptor channels. Knowledge of the primary structures of Kir channels and the ability to mutate them also has led to the determination of many of the structural requirements of inward rectification.
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            Observations in experimental magnesium depletion.

            R Whang, L Welt (1963)
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              Studies on the pathogenesis of Bartter's syndrome.

              There is no agreement concerning the primary pathogenetic event leading to Bartter's syndrome. Free water clearance and distal fractional chloride reabsorption were abnormally low in our patient with Bartter's syndrome. This series of investigations in this patient with Bartter's syndrome and hypomagnesemia was undertaken to determine if the defect in chloride transport in the ascending limb and the associated renal potassium wasting was specifically related to potassium depletion, increased prostaglandin production or magnesium depletion. Neither potassium repletion, indomethacin administration nor magnesium repletion had an effect on the defect in free water clearance or in distal fractional chloride reabsorption. However, magnesium infusion eliminated renal potassium wasting. These observations suggest that the proximate cause of Bartter's syndrome in this patient is a primary defect in the reabsorption of sodium chloride in the ascending limb and not renal potassium wasting. however, hypomagnesemia may contribute to the renal potassium wasting seen in this syndrome.
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                Author and article information

                Journal
                Journal of the American Society of Nephrology
                JASN
                American Society of Nephrology (ASN)
                1046-6673
                1533-3450
                September 26 2007
                October 2007
                October 2007
                September 05 2007
                : 18
                : 10
                : 2649-2652
                Article
                10.1681/ASN.2007070792
                17804670
                b5d54aa9-2625-4296-a88b-949569563953
                © 2007
                History

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