When EGF is offside, magnesium is wasted
J. Clin. Invest. Shmuel Muallem, et al. 117:2086 doi:10.1172/JCI33004 [Go to this article.]

Figure 1
Renal Mg²⁺ handling. Non–protein bound Mg²⁺ is filtered freely at the glomerulus, and the approximate percentages of filtered Mg²⁺ absorbed at different locations are shown. Under most physiologic conditions, about 10% of filtered Mg²⁺ is excreted. The final regulatory segment, the DCT, controls approximately 5% of filtered Mg²⁺. Mg²⁺ is transported by both the paracellular and transcellular pathways. Four monogenic diseases that lead to renal Mg²⁺ wasting as a result of mutations in the genes coding for the proteins shown in red have been described to date. Mutations in paracellin-1 and claudin-19 are involved in familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC). Mutations in TRPM6 are involved in HSH. Mutations in NaCl cotransporter are involved in Gitelman syndrome, and mutations in the γ subunit of Na,K-ATPase are involved in autosomal dominant renal hypomagnesemia with hypocalciuria (ADRHH). The question mark indicates unknown pathways; the numbers 1.5, 0.6, and 0.8 indicate Mg²⁺ concentrations in moles in the lumen of the respective segment. NKCC2, Na,K-2Cl^– cotransporter.