Abstract: FR-PO161
Noncontrast Resting State Magnetic Resonance Imaging Measures Tubuloglomerular Feedback Function and Detects Functional Changes after AKI
Session Information
- AKI: Mechanisms
October 25, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Baldelomar, Edwin, Washington University in St Louis School of Medicine, St Louis, Missouri, United States
- Charlton, Jennifer R., University of Virginia School of Medicine, Charlottesville, Virginia, United States
- Bennett, Kevin M., Washington University in St Louis School of Medicine, St Louis, Missouri, United States
Background
The tubuloglomerular feedback (TGF) is a critical autoregulatory mechanism that plays a significant role in modulating single nephron filtration and hyperfiltration in response to acute kidney injury (AKI). There are no clinical tools to measure TGF. Noncontrast resting state magnetic resonance imaging (rsMRI) has recently been used to detect hemodynamic fluctuations in the kidney, potentially linked with autogregulation. Here, we investigated if fluctuations (0.02-0.05 Hz) measured by rsMRI reflect TGF. We further tested if rsMRI detects changes in fluctuations, reflecting function, after AKI that are not detected by standard metrics.
Methods
TGF study – rsMRI was performed during saline infusion (20μl/min, 30min, baseline) and furosemide infusions (20μg/mL, ~45min) on male Sprague Dawley (SD) rats (N=4). AKI study – For AKI injury, female SD rats were stratified to folic acid (FA, 200 mg/kg) or sodium bicarbonate(N = 9). rsMRI was performed prior to AKI and again at 10, and 36 day after FA. Transcutaneous GFR, sCr, and BUN were measured days 3 and 59. rsMRI spectra were computed as published. Significance (t-test) at p<0.05.
Results
TGF study, Figure 1A-B - Furosemide attenuated the rsMRI spectral peaks at 0.015-0.05Hz in cortex. Power in this band was ~60% lower after furosemide, and 70% fewer voxels had a peak in that band. AKI Study, Fig1C-D - AKI was confirmed on day 3 after AKI. On day 36, the distribution of power between 0.015-0.055Hz in cortex, and distribution of power between 0.055-0.1 Hz in outer medulla were lower in the FA group. There was no difference in GFR, or BUN and creatinine 3 and 59 days after AKI.
Conclusion
TGF can be measured using noncontrasted rsMRI. Changes in TGF after AKI remain present despite normalization of renal function. This suggests rsMRI could be a translatable tool to understand the role of TGF in disease progression after AKI or in response to therapies.
Funding
- NIDDK Support