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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Obesity and type 2 diabetes (T2D) are rising globally and can precipitate kidney injury long before overt chronic kidney disease (CKD). Multiparametric kidney MRI non-invasively profiles kidney structure and function, offering a window into early pathophysiology; however, contemporary and multi-ethnic datasets in this population remain limited.
We analyzed youth and young adults with obesity and T2D from Renal HEIR (RH) and its follow-up/extension, Renal HEIRitage (RH2), to characterize stage-dependent changes in kidney function and oxygenation. Two ancillary cohorts were used only where specified to support phenotype and medication analyses: IMPROVE (T2D only; n=21; mean±SD age 17±2 years; BMI 46±8 kg/m2) and PANTHER (normal weight controls, n=48; and participants with obesity and T2D, n=72; age 12±2 years; BMI 33±6 kg/m2). RH enrolled adolescents with normal weight, obesity, or T2D using harmonized kidney measures and multiparametric MRI; RH2 was a follow-up cohort that also enrolled new participants under the same inclusion criteria as RH. Assessments included iohexol-measured glomerular filtration rate (GFR) and estimated GFR, p-aminohippurate (PAH) clearance to estimate renal plasma flow (RPF), urinary albumin-to-creatinine ratio (UACR), and kidney MRI metrics: total kidney volume (TKV), apparent transverse relaxation rate (R2*), and medullary furosemide-suppressible oxygen consumption (FSOC) derived from blood oxygenation level dependent (BOLD) MRI. For R2* comparisons, participants with obesity and T2D were classified as CKD (eGFR <75 mL/min/1.73 m2and/or UACR ≥100 mg/g) or non-CKD (eGFR ≥75 mL/min/1.73 m2 and UACR <100 mg/g). Medullary FSOC was compared across normal weight, obesity, and T2D; within T2D, we examined differences by exposure to sodium–glucose cotransporter-2 inhibitors (SGLT2i).
Measured GFR was higher in RH than RH2 (165±40 vs 120±28 mL/min per1.73 m2; p<0.001), consistent with shorter diabetes duration (2±2 vs 12±10 years; p<0.001) and earlier disease stage; RPF was likewise higher in RH. Height-adjusted TKV was smaller in RH than RH2 (197±36 vs 242±55 mL/m; p<0.001), consistent with progression from hyperfiltration to structural enlargement. Average kidney R2* was lower in RH compared with RH2 (20±2 vs 23±4 S-1; p<0.001), suggesting a shift from relative hyperoxia toward hypoxia with advancing stage. Across CKD strata, R2* was significantly higher in CKD than non-CKD after adjusting for BMI categories, diabetes status, and age (p=0.003; Figure 2). In medullary FSOC comparisons (Figure 3), obese controls and T2D exhibited lower FSOC than lean controls, reaching significance for obese vs lean (p<0.001). Notably, T2D exhibited higher medullary FSOC than obese (p=0.038). Among T2D, SGLT2i exposure was associated with higher medullary FSOC compared with no SGLT2i (p=0.036; Figure 4).
Multiparametric kidney MRI sensitively captures stage-dependent hemodynamics, structural change, and oxygenation in obesity and T2D. SGLT2 inhibition demonstrates reversal of abnormal renal oxygenation, evidenced by favorable changes in medullary FSOC. These findings support multiparametric MRI as a non-invasive biomarker suite to track progression and therapeutic response in early diabetic kidney disease.
