ArticleBiochemistry and biophysics reports2026
Renoprotective effects of gut NHE3 inhibitor tenapanor in a rat model of unilateral renal ischemia-reperfusion injury with contralateral nephrectomy.
Article in Biochemistry and biophysics reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Kidney ischemia-reperfusion (I/R) injury is an unavoidable complication of kidney transplantation that contributes to acute kidney injury (AKI), chronic kidney disease (CKD), and limited long-term graft survival. Elevated serum phosphate has been implicated not only as a consequence of renal dysfunction but also as an active mediator of kidney injury. Tenapanor, an intestinal sodium/hydrogen exchanger 3 inhibitor approved for the treatment of hyperphosphatemia in dialysis patients, may therefore have renoprotective potential; however, its effects on renal I/R injury remain unclear. Here, we show that oral administration of tenapanor suppresses renal calcium phosphate deposition after I/R, mitigates AKI progression, and reduces subsequent renal fibrosis in rats. These findings suggest that tenapanor mitigates renal I/R injury and may represent a potential pre-transplant strategy to improve long-term graft outcomes.
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