β-Hydroxybutyrate: a renoprotective hormone in polycystic kidney disease.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical mechanisms and early clinical literature without systematic search methodology.
PubMed 42530143 · doi:10.1152/ajpendo.00067.2026
What was done
This narrative review summarizes preclinical and early clinical research on ketogenic metabolic therapy (including ketogenic diets, intermittent fasting, time-restricted feeding, and β-hydroxybutyrate supplementation) and the mechanistic role of β-hydroxybutyrate (BHB) in autosomal dominant polycystic kidney disease (ADPKD).
What was found
The abstract reports no numerical findings or statistical estimates. It reports qualitatively that ADPKD involves mitochondrial dysfunction and reliance on glucose metabolism, and that BHB functions as an alternative energy substrate and pleiotropic signaling hormone that reduces cyst proliferation, inflammation, oxidative stress, and fibrosis.
Why it matters
Pharmacological therapies for ADPKD remain limited. Framing BHB and ketogenic metabolic therapy as targeted interventions identifies potential non-invasive strategies to modify metabolic dysfunction in polycystic kidney disease.
Limits
As a narrative review, it lacks systematic search criteria, quality appraisal, and meta-analytic synthesis. The abstract presents no quantitative clinical outcome data, sample sizes, or details on long-term safety and renal preservation in humans.
Cited by
- context The kidney nephron uses ketones as its primary fuel rather than glucose.