Abstract: SA-PO0556
Intraglomerular Hemodynamic Function and Cyst Burden in Adults with ADPKD
Session Information
- Cystic Kidney Diseases: Clinical Research
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Genetic Diseases of the Kidneys
- 1201 Genetic Diseases of the Kidneys: Monogenic Kidney Diseases
Authors
- Narongkiatikhun, Phoom, University of Washington School of Medicine, Seattle, United States
- Gitomer, Berenice Y., University of Colorado Anschutz Medical Campus School of Medicine, Aurora, Colorado, United States
- Kline, Timothy L., Mayo Clinic College of Medicine and Science, Rochester, Minnesota, United States
- Choi, Ye Ji, University of Washington School of Medicine, Seattle, Washington, United States
- Chonchol, Michel, University of Colorado Anschutz Medical Campus School of Medicine, Aurora, Colorado, United States
- Pinzon Cortes, Jairo Arturo, University of Washington School of Medicine, Seattle, Washington, United States
- Hampson, Hailey E, University of Washington School of Medicine, Seattle, Washington, United States
- Tommerdahl, Kalie L., University of Washington School of Medicine, Seattle, Washington, United States
- Pyle, Laura, University of Washington School of Medicine, Seattle, Washington, United States
- Nowak, Kristen L., University of Colorado Anschutz Medical Campus School of Medicine, Aurora, Colorado, United States
- Bjornstad, Petter, University of Washington School of Medicine, Seattle, Washington, United States
Background
ADPKD is characterized by progressive cyst growth and structural remodeling. The disease features altered kidney hemodynamics, but the interrelationships between intraglomerular pressure, renal perfusion, and cyst burden remain incompletely characterized, limiting our understanding of potential therapeutic targets.
Methods
This observational study included 20 adults with ADPKD enrolled in the PENGUIN study. Participants underwent plasma clearance of iohexol and para-aminohippurate (PAH) to determine measured glomerular filtration rate (mGFR), renal plasma flow (RPF), and derived intraglomerular hemodynamic parameters. Kidney structure was assessed by multiparametric MRI, and 11C-acetate PET was used to quantify cortical perfusion. Pearson correlation coefficients evaluated associations between kidney hemodynamic parameters and imaging-derived structural and metabolic markers, with significance set at p<0.05.
Results
Participants (mean[±SD] age 31±6 years; 65% women) had preserved kidney function (mean mGFR 107±20 mL/min per 1.73 m2) with mean height-adjusted total kidney volume [HtTKV] of 731±370 mL/m. Greater HtTKV (r:-0.60, p<0.01), total cyst volume (r:-0.61, p<0.01) and cyst surface area (r:-0.47, p<0.05) associated with lower intraglomerular pressure. This relationship was likely mediated by significantly higher afferent arteriolar resistance (r:0.53 for HtTKV; r:0.51 for total cyst volume; r:0.53 for cyst surface area; all p<0.05) and reduced cortical perfusion (r:-0.48, p<0.05) in the setting of higher cyst burden.
Conclusion
In ADPKD, greater cyst burden associated with altered intraglomerular hemodynamic function characterized by increased afferent arteriolar resistance, reduced cortical perfusion and attenuated intraglomerular pressure, likely secondary to the effects of mechanical compression. These findings suggest that therapies targeting the vasculature to counteract elevated afferent arteriolar resistance may have therapeutic potential. Agents that selectively reduce afferent arteriolar tone, such as calcium channel blockers or endothelin receptor antagonists, might help normalize glomerular hemodynamics in ADPKD.