Abstract: FR-PO119
Serial Multiparametric Kidney Magnetic Resonance Imaging in a Prospective Cohort of Patients with AKI
Session Information
- AKI: Diagnosis and Outcomes
October 25, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Noble, Rebecca Anne, University Hospitals of Derby and Burton NHS Foundation Trust, Derby, United Kingdom
- Cox, Eleanor F., University of Nottingham, Nottingham, United Kingdom
- Taal, Maarten W., University Hospitals of Derby and Burton NHS Foundation Trust, Derby, United Kingdom
- Selby, Nicholas M., University Hospitals of Derby and Burton NHS Foundation Trust, Derby, United Kingdom
- Francis, Susan, University of Nottingham, Nottingham, United Kingdom
Background
Recovery from acute kidney injury (AKI) is traditionally measured using serum creatinine but this often over-estimates the degree of renal recovery. Magnetic resonance imaging (MRI) is an imaging modality with promise to improve the understanding and characterisation of renal pathophysiology. In a single renal multiparametric MRI (mpMRI) scan, measures can assess renal morphology, tissue microstructure, oxygenation, perfusion and blood flow. This study aimed to assess the degree of change between 30- and 90-days post AKI, as the first 90 days after AKI appear to be the important in terms of determining outcomes.
Methods
Prospective observational study of 10 participants with AKI of all stages recruited at the time of AKI and followed up with monthly blood and urine samples. MRI scans collected on a Philips 3T Ingenia at Visit 1 (V1, 30-60 day) and Visit 2 (V2, day 90). The MRI protocol included: T2-weighted scans for total kidney volume (TKV), T1 and T2 mapping, DWI, ASL, phase contrast MRI, TRUST-MRI and BOLD T2*.
Results
Participants (5M:5F, median age 64y (IQR 54–68)) had predominantly severe AKI (n=5 stage 3, n=4 stage 2, n=1 stage 1, with median baseline eGFR 82ml/min/1.73m2 (60-89)) and were heterogeneous in terms of AKI aetiology and subsequent recovery.
At V1, 7/10 participants had elevated cortex T1 compared to the healthy range (mean group T1 at V1: 1606±89ms), 3 of these 7 participants returned to the healthy range by V2 (group T1 at V2: 1551±83ms). 3 participants had reduced T2 at V1 compared to the healthy range (group average 99.7±8ms at V1, and group average 100±5ms at V2). Those participants who did not recover renal function at V2 typically had higher T1 and lower T2 at V1, with a trend towards the healthy range at V2.
Conclusion
We observed different patterns of MRI parameter change after AKI which appear to relate to the degree of kidney damage: high T1 suggesting more inflammation and/or oedema and a low T2 suggesting a greater degree of hypoxia. Further analysis will explore how these MRI changes are related to other markers of kidney damage.