Kidney stones are very common and on the rise worldwide. Calcium oxalate stones are the most common kidney stones. Oxalate homeostasis is achieved through a balance of endogenous synthesis and oral uptake versus kidney and gut oxalate excretion. We here propose to investigate the role of the anion transporter SLC26A2 in oxalate homeostasis by (1) Generating SLC26A2-deficient human gut and kidney organoids and mice with gut-specific knockout of SLC26A2. (2) Investigating gut transport processes using transport studies in human gut organoids and mucosa preparations from mice. (3) Examining renal transport processes in vitro and in vivo. (4) Characterizing the role of SLC26A2 in preventing hyperoxalemia in a model of chronic kidney disease.
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