When the kidneys fail the gastrointestinal tract adapts and aids in electrolyte balance. Examples include increased fecal potassium excretion in patients with kidney disease. Similarly, it has been demonstrated that the intestine can increase fecal oxalate excretion in patients with chronic kidney disease. Oxalate is toxin that upon accumulation in the body can harm various organs. However, the molecular identity of the transport processes responsible for increased oxalate excretion in the intestine in states of kidney disease has been unknown.
Researchers from Charite, Friedrich-Alexander-Universität Erlangen-Nürnberg and Yale University revealed that intestinal expression of oxalate transporter Slc26a6 is strongly upregulated in murine models of CKD. Deletion of Slc26a6 completely abrogates the enhanced fecal oxalate excretion, resulting in increased plasma oxalate concentration. The results demonstrate that Slc26a6 plays a critical role in mediating intestinal oxalate secretion and mitigating hyperoxalemia in kidney disease. Moreover, the findings of the investigators suggest that Slc26a6 might be a good candidate for pharmacological approaches to prevent hyperoxalemia in CKD. The complete findings of Laura Neumeier, a former doctoral student of the DAAD – TRENAL („Translational kidney research – from physiology to clinical application“) program, and colleagues, will be published soon in the Journal of the American Society of Nephrology (JASN).