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Claudin-16 is an integral membrane protein encoded by the CLDN16 gene and a core component of tight junctions in the kidney, specifically in the thick ascending limb of Henle’s loop. It forms paracellular channels (often in complex with Claudin-19) that selectively allow cations such as magnesium and calcium to pass between epithelial cells, crucial for maintaining electrolyte balance and generating the transepithelial voltage needed for passive reabsorption of these ions. Mutations or functional disruption of Claudin-16 impair paracellular magnesium and calcium resorption, leading to severe renal magnesium wasting, hypercalciuria, nephrocalcinosis, and progressive kidney failure—a condition known as familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC). No drugs directly target Claudin-16; its clinical significance is primarily as a genetic and functional biomarker for certain genetic forms of kidney disease[1][2][3][4].
Not applicable; no known drugs directly target Claudin-16. Theoretical mechanisms would involve modulation of paracellular permeability or ion channel formation within tight junctions.
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