Evaluation of renal oxygenation by BOLD-MRI in high-risk patients with type 2 diabetes and matched controls

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BACKGROUND: Diabetic kidney disease (DKD) accounts for approximately 50% of end-stage kidney disease. Renal hypoxia is suggested as a main driver in the pathophysiology underlying chronic DKD. Blood Oxygenation Level Dependent Magnetic Resonance Imaging (BOLD-MRI) has made non-invasive investigations of renal oxygenation in humans possible. Whether diabetes per se contributes to measurable changes in renal oxygenation by BOLD-MRI remains to be elucidated. We investigated whether renal oxygenation measured with BOLD-MRI differs between people with type 2 diabetes (T2DM) with normal to moderate chronic kidney disease (CKD) (Stages 1-3A) and matched controls. The repeatability of the BOLD-MRI method was also assessed.

METHODS: In this matched cross-sectional study, 20 people with T2DM (age 69.2 ± 4.7 years, duration of diabetes 10.5 ± 6.7 years, Male 55,6%) and 20 matched non-diabetic controls (Mean age 68.8 ± 5.4 years, Male 55,6%). underwent BOLD-MRI analyzed with the Twelve layer concentric object method. To investigate the repeatability, 7 in the T2DM group and 9 in the control group were scanned twice.

RESULTS: A significant reduction in renal oxygenation from cortex to medulla was found in both groups P < 0.01, no inter-group difference was detected (0.71[s-1], [95% CI; (-0.28;1.7 s-1)], P = 0.16). Median intra individual coefficient of variation (CV) varied from 1.2% to 7.0%.

CONCLUSION: T2DM patients with normal to moderate CKD does not seem to have lower renal oxygenation when measured with BOLD-MRI and TLCO. BOLD-MRI has a low intra-individual CV and seems like a reliable method for investigation of renal oxygenation in T2DM.

OriginalsprogEngelsk
TidsskriftNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
ISSN0931-0509
DOI
StatusE-pub ahead of print - 24 maj 2022

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© The Author(s) 2022. Published by Oxford University Press on behalf of the ERA.

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