Jacob Torres, Elizabeth Sharpe and Thomas Weimbs (UC Santa Barbara) published a review on July 30, 2026 in the American Journal of Physiology - Endocrinology and Metabolism making the case that β-hydroxybutyrate (BHB) is the principal renoprotective mediator behind ketogenic metabolic therapy in ADPKD.
The argument starts from the now well-supported view of ADPKD as a metabolic disease at the cellular level: cyst-lining cells show impaired mitochondrial function and a pathological reliance on glucose metabolism. Ketogenic metabolic therapy — ketogenic diets, intermittent fasting, time-restricted feeding, or exogenous BHB supplementation — targets that vulnerability.
The authors describe BHB as doing more than substituting for glucose as fuel. They summarize evidence that BHB acts as a signaling molecule with pleiotropic effects: reduced cyst proliferation, inflammation, oxidative stress and fibrosis, alongside improved mitochondrial function. On that basis they characterize it as a renoprotective hormone rather than a metabolic byproduct.
The review also notes that modern dietary and lifestyle patterns chronically suppress endogenous ketogenesis, which may deprive tissues of BHB's signaling functions. That framing matters practically: it is the rationale for exogenous ketone products such as KetoCitra and for the ketone-supplement trials now running, since the benefit is attributed to BHB exposure rather than to carbohydrate restriction per se. As a narrative review, it synthesizes existing evidence rather than reporting new trial data.