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Background  A state of oxalate homeostasis is maintained in patients with healthy kidney function. However, as GFR declines, plasma oxalate (P ox ) concentrations start to rise. Several groups of researchers have described augmentation of oxalate secretion in the colon in models of CKD, but the oxalate transporters remain unidentified. The oxalate transporter Slc26a6 is a candidate for contributing to the extrarenal clearance of oxalate  via  the gut in CKD.    Methods  Feeding a diet high in soluble oxalate or weekly injections of aristolochic acid induced CKD in age- and sex-matched wild-type and  Slc26a6   −/−   mice. qPCR, immunohistochemistry, and western blot analysis assessed intestinal  Slc26a6  expression. An oxalate oxidase assay measured fecal and P ox  concentrations.    Results  Fecal oxalate excretion was enhanced in wild-type mice with CKD. This increase was abrogated in  Slc26a6   −/−   mice associated with a significant elevation in plasma oxalate concentration.  Slc26a6  mRNA and protein expression were greatly increased in the intestine of mice with CKD. Raising P ox  without inducing kidney injury did not alter intestinal  Slc26a6  expression, suggesting that changes associated with CKD regulate transporter expression rather than elevations in P ox .    Conclusions  Slc26a6-mediated enteric oxalate secretion is critical in decreasing the body burden of oxalate in murine CKD models. Future studies are needed to address whether similar mechanisms contribute to intestinal oxalate elimination in humans to enhance extrarenal oxalate clearance.

Enteric Oxalate Secretion Mediated by Slc26a6 Defends against Hyperoxalemia in Murine Models of Chronic Kidney Disease