Beta-hydroxybutyrate restores OXPHOS to reduce  ischemia-induced AKI
Bilateral renal ischemia-reperfusion injury (IRI) induces acute kidney injury (AKI) and impairs mitochondrial energy metabolism in renal tubules. While ketogenic diets rich in beta-hydroxybutyrate (BHB) are known to confer tissue protection, we investigated the specific effect of BHB sodium pretreatment in this model. Mice subjected to bilateral IRI with or without BHB sodium pretreatment were assessed 24 hours post-reperfusion. Our results demonstrate that BHB administration restored oxidative phosphorylation (OXPHOS) and attenuated injury in post-ischemic AKI. These findings indicate that BHB enhances OXPHOS capacity within the electron transport chain, thereby regulating mitochondrial energy metabolism and ameliorating ischemia-induced AKI.