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Based on genetic studies in families with hereditary renal Mg(2+) reabsorption disorders, several genes were shown to be involved in renal Mg(2+) transport. Mutations in the CLDN16 gene were found to underlie autosomal recessive hypomagnesaemia associated with hypercalciuria and nephrocalcinosis. The FXYD2 gene was implicated in autosomal dominant renal Mg(2+) wasting associated with hypocalciuria. Mutations in the SLC12A3 gene, also known as NCC, cause Gitelman's syndrome. In addition to hypokalaemic metabolic alkalosis, hypomagnesaemia associated with hypocalciuria is considered to be a hallmark feature of this latter disorder.

Exclusion of mutations in FXYD2, CLDN16 and SLC12A3 in two families with primary renal Mg2+ loss