Abstract: FR-PO068

Assessment of the Pathophysiology of AKI Using Magnetic Resonance Imaging

Session Information

  • AKI Clinical: Predictors
    November 03, 2017 | Location: Hall H, Morial Convention Center
    Abstract Time: 10:00 AM - 10:00 AM

Category: Acute Kidney Injury

  • 003 AKI: Clinical and Translational

Authors

  • Mahmoud, Huda, Center for Kidney Research and Innovation, Derby, United Kingdom
  • Buchanan, Charlotte Elizabeth, Sir Peter Mansfield Imaging Centre, Nottingham, United Kingdom
  • Cox, Eleanor, Sir Peter Mansfield Imaging Centre, Nottingham, United Kingdom
  • Prestwich, Benjamin L, Sir Peter Mansfield Imaging Centre, Nottingham, United Kingdom
  • Taal, Maarten W., Center for Kidney Research and Innovation, Derby, United Kingdom
  • Francis, Susan, Sir Peter Mansfield Imaging Centre, Nottingham, United Kingdom
  • Selby, Nicholas M., Center for Kidney Research and Innovation, Derby, United Kingdom
Background

The pathophysiology of Acute Kidney Injury(AKI) in humans is not well delineated, in part due to limitations in current methods of renal imaging. Recent advances in Magnetic Resonance Imaging(MR) allow assessment of structural and functional changes relevant to kidney disease. We performed a multiparametric MR study to assess its utility and reproducibility in patients with AKI.

Methods

We studied 9 patients with AKI stage2/3(with no pre-existing CKD) and 13 healthy volunteers(HV). Patients underwent multiparametric renal MR scans at the time of AKI and 90d later.
MR scans were performed on a 3T Philips Ingenia scanner. Structural assessments included renal volume, longitudinal-relaxation time(T1) and Diffusion-Weighted Imaging(DWI) as markers of fibrosis and/or inflammation. Functional assessments included Arterial Spin Labelling(ASL) to measure renal perfusion and Blood Oxygenation Level Dependant Imaging(BOLD) as an indicator of renal oxygenation.

Results

AKI patients: mean 47±19yrs, baseline creatinine 78±14µmol/L, peak creatinine 467±254µmol/L. All achieved complete biochemical recovery(creatinine 88±17µmol/L) and 5 have had repeat scans at 90d.
Renal volumes were significantly increased at time of AKI as compared to HVs(270±92ml vs 189±25ml respectively p=0.001). BOLD T2*, cortical and medullary T1 values were significantly increased in AKI patients at the time of injury compared to HVs.
90d post AKI renal volumes had reduced(210±75ml p=0.04), as had T2*, cortical and medullary T1 values. T1 values at 90d remained significantly higher than the HVs(p<0.001).

Conclusion

This is the first study to use multiparametric MR in patients with AKI, assessing kidney function and structure at time of AKI and during recovery. The increase in renal volumes and T1 values at time of AKI may be indicate inflammation or oedema. The persistent increase in T1 at 90d may represent persistent inflammation or fibrosis development. Importantly, persistent MR abnormalities at 90d despite complete biochemical normalisation show the potential of MR to better characterise recovery. Further studies are required to build on this initial pilot work, and determine how best multiparametric MR can be used to characterise the nature of renal injury in AKI and its recovery.

Funding

  • Private Foundation Support