Study Design
Narrative review (published July 30, 2026) synthesizing preclinical and clinical evidence on Ketogenic Metabolic Therapy (KMT) in ADPKD and on β-hydroxybutyrate (BHB) as the mediator of its effects.
Intervention
Covers the full range of KMT approaches: ketogenic diets, intermittent fasting, time-restricted feeding, and supplementation with exogenous BHB.
Key Results
Core Thesis: BHB is the mediator
The authors argue accumulating evidence points to BHB as the principal renoprotective mediator behind the benefits of ketogenic metabolic therapy — a signaling hormone, not merely an alternative fuel.
Metabolic Defect: Glucose dependence
ADPKD is characterized at the cellular level by impaired mitochondrial function and a pathological reliance on glucose metabolism — the vulnerability KMT targets.
BHB Signaling: Pleiotropic
Beyond fuel, BHB is described as reducing cyst proliferation, inflammation, oxidative stress and fibrosis while enhancing mitochondrial function.
Modern Diets: Ketogenesis suppressed
Chronic suppression of endogenous ketogenesis is common in modern societies due to dietary and lifestyle patterns, potentially depriving tissues of BHB's signaling functions.
Context & Comparison
Complements the 2026 systematic review of ketogenic interventions in ADPKD by shifting focus from the diet as a whole to BHB as the specific active molecule — the rationale behind exogenous ketone products such as KetoCitra and behind the ketone-supplement RCTs now underway.
Significance
This review comes from the lab that produced the original preclinical ADPKD ketosis work (Torres et al., Cell Metabolism 2019). It frames BHB as a renoprotective signaling hormone and positions ketogenic metabolic therapy — whether by diet, fasting, or exogenous BHB — as a safe, non-invasive and potentially disease-modifying intervention in ADPKD. As a narrative review it synthesizes existing evidence rather than adding new trial data.