Abstract: SA-PO0115
Improvement from Stage 4 to Stage 3b CKD in ADPKD After Ketogenic Metabolic Therapy and Supplementation with Exogenous Ketones and Alkaline Citrate: A Case Study
Session Information
- ADPKD and Cystic Kidney Disease - 3
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Genetic Diseases of the Kidneys
- 1201 Genetic Diseases of the Kidneys: Cystic (Monogenic)
Authors
- Messing, Melina, University of California Santa Barbara, Santa Barbara, California, United States
- Muensterman, Emily Grace, Santa Barbara Nutrients Inc, Santa Barbara, California, United States
- Weimbs, Thomas, University of California Santa Barbara, Santa Barbara, California, United States
Introduction
ADPKD is a progressive genetic disorder characterized by cyst growth and declining kidney function. Emerging evidence suggests ketogenic metabolic therapy (KMT) may be therapeutic in mild-to-moderate ADPKD, but its efficacy in advanced CKD remains uninvestigated. We report substantial kidney function improvement in a 66-year-old female with advanced ADPKD enrolled in the Ren-Nu™ KMT program.
Case Description
A 66-year-old female with advanced ADPKD participated in tolvaptan clinical trials and remained on tolvaptan for approximately 18 years. Despite treatment, eGFR declined from 32 mL/min/1.73m2 (2023) to 20 mL/min/1.73m2 (June 2025). She enrolled in Ren-Nu™ in August 2025, continuing tolvaptan throughout. Ren-Nu™ is a structured KMT program including daily KetoCitra® supplementation (beta-hydroxybutyrate, alkaline citrate, and minerals), individualized nutritional guidance, ketosis monitoring, and kidney-safe nutrition education.
Following initiation of the program, kidney function improved substantially. From June to December 2025, serum creatinine decreased from 2.62 mg/dL to 1.90 mg/dL, while cystatin C decreased from 2.26 mg/L to 1.72 mg/L. The combined creatinine–cystatin C eGFR improved from 21.8 to 32.2 mL/min/1.73m2, representing a clinically meaningful transition from CKD Stage 4 to Stage 3b over six months. Additional laboratory improvements included reductions in blood urea nitrogen (46 to 26 mg/dL), phosphorus (4.5 to 3.4 mg/dL), and uric acid (8.8 to 7.6 mg/dL). Hemoglobin A1c decreased from 5.3% to 5.0%, while albumin and potassium remained stable and within normal ranges throughout the intervention. The patient additionally reported marked improvements in overall well-being, energy levels, and quality of life.
Discussion
This case demonstrates that meaningful improvement in kidney function may still be achievable in later-stage ADPKD through KMT, even in a patient with longstanding disease, advanced CKD, and prolonged tolvaptan use. These findings support further investigation of KMT as a complementary therapeutic strategy in advanced ADPKD.