A new study shows that Slc26a6-null mice manifest calcium-oxalate nephrolithiasis accompanied by enhanced net intestinal oxalate absorption. These findings point to a critical role for Slc26a6 in gastrointestinal oxalate secretion and suggest a genetic explanation for a common form of renal stone disease in humans.
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Kleta, R. A key stone cop regulates oxalate homeostasis. Nat Genet 38, 403–404 (2006). https://doi.org/10.1038/ng0406-403
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DOI: https://doi.org/10.1038/ng0406-403
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