Familial hypercalciuric hypomagnesemia with nephrocalcinosis (FHHNC) is an autosomal recessive disorder with mutations in the genes encoding claudin 16 and 19. Loop diuretics by inhibiting NKCC2 therefore result in increased magnesium excretion. This is required for the paracellular permeability of divalent cations like magnesium and calcium. With continuous NaCl reabsorption along TAL, a lumen positive voltage gradient is created. Chloride leaves the cell through the basolateral membrane via chloride channels. In this exchange, potassium that has entered the cell is secreted into the lumen through the renal outer medullary potassium channel. Sodium then exits the cell through Na/K ATPase present at the basolateral membrane. In TAL, sodium, potassium, and chloride enter the cell through Na-K-2Cl contransporter (NKCC2) in the luminal membrane. There are two conditions required for magnesium reabsorption in TAL: first is a lumen positive transepithelial voltage and second is paracellular permeability for the divalent cations. The process of reabsorption of magnesium in the thick ascending loop is facilitated by paracellin-1/claudin 16 and claudin 19 belonging to the claudin protein family. Hypomagnesemia in patients with familial hypomagnesemia with secondary hypocalcemia has been attributed to mutations of TRPM6. Although the mechanism of regulatory factors driving magnesium absorption is not clear, intestinal absorption is not directly proportional to dietary intake but is also dependent on magnesium status in the body.Ī lower dietary magnesium intake will lead to reliance on active transcellular uptake via magnesium-specific transporters in the large intestine, namely, TRPM6 and TRPM7. Active transport is facilitated by transient receptor potential channel melastatin member 6 (TRPM6) and TRPM7 Mg 2+ channels. The exact mechanism for paracellular transport is not known but has been attributed to high luminal magnesium concentration and tight junction permeability regulated by claudins. Paracellular absorption is the passive transport which is responsible for 80–90% of uptake. There are two pathways, namely, paracellular and transcellular, for magnesium absorption. Understanding the physiological aspects is important to guiding the management of magnesium disorders.īased on literature review, magnesium is absorbed mostly in the small intestine and to some extent in the large intestine. The cause of hypomagnesemia depends primarily on alterations in intake, redistribution, and excretion. In hospitalized patients, the risk is the highest for intensive care unit (ICU) patients. The reported incidence of hypomagnesemia is approximately 2% in the general population. The reported incidence of hypomagnesemia is likely less than expected. Some studies estimate that approximately three-fourths of Americans do not take the recommended dietary allowance of magnesium. The reason for it not getting the needed attention is because of rare symptomatology until levels are really low and also because of a lack of proper understanding of magnesium physiology. The importance of magnesium is well known, but still it is the forgotten electrolyte. It plays an important role in molecular, biochemical, physiological, and pharmacological functions in the body. Magnesium is one of the most abundant cation in the body as well as an abundant intracellular cation.
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