Secondary Mg Deficiency

Failure of the mechanisms that ensure Mg home-ostasis, or endogenous or iatrogenic perturbing factors of Mg status, leads to secondary Mg deficit. Secondary Mg deficiency requires a more or less specific correction of its causal dysregulation.

Intestinal Mg absorption decreases in the case of malabsorption syndromes, such as chronic diarrhoea, inflammatory enteropathy, intestinal resection, and biliary and intestinal fistulas.

Hypermagnesuria is encountered in the case of metabolic and iatrogenic disorders, such as primary and secondary hyperaldosteronism (extracellular volume expansion), hypercalcemia (competition Ca/Mg at the thick ascending loop of Henle), hyper-parathyroidism, and phosphate or potassium depletion. Hypermagnesuria may also result from tubulopathy, as the selective defect of the Mg tubular reabsorption (chromosome 11q23), Bartter's syndrome (thick ascending loop of Henle), or Gitelman's syndrome (distal convoluted tubule).

Administration of medications can be a causal factor in the development of secondary Mg deficiency. Administration of diuretics is the main cause of iatrogenic deficit because it decreases NaCl reabsorption in the thick ascending loop of Henle and thus increases the fractional excretion of Mg.

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