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Kidney Week

Abstract: TH-PO1126

Use of Multi-Parametric Functional MRI to Identify Progressive CKD

Session Information

Category: CKD (Non-Dialysis)

  • 1902 CKD (Non-Dialysis): Clinical, Outcomes, and Trials


  • Li, Luping, NorthShore University HealthSystem, Evanston, Illinois, United States
  • Li, Wei, NorthShore University HealthSystem, Evanston, Illinois, United States
  • Hack, Bradley K., NorthShore University HealthSystem, Evanston, Illinois, United States
  • Kohn, Orly F., Pritzker School of Medicine, University of Chicago, Chicago, Illinois, United States
  • Sprague, Stuart M., NorthShore University HealthSystem, Evanston, Illinois, United States
  • Prasad, Pottumarthi V., NorthShore University HealthSystem, Evanston, Illinois, United States

Only a quarter of those with stage 3 CKD will progress to end stage kidney disease over 10 years [PMID: 22545920]. Hence, there is a need for novel markers to identify individuals at risk of progressive CKD. The chronic hypoxia hypothesis suggests that progressive CKD involves loss of peritubular capillaries leading to hypoxia which results in development of fibrosis [PMID: 25401039]. MRI can evaluate perfusion, oxygenation and fibrosis using arterial spin labeling, blood oxygenation level dependent (BOLD) and diffusion MRI respectively. We evaluated a cohort of diabetic patients with CKD stage 3 using these three techniques to determine whether we can identify patients at risk of progressive CKD.


41 patients (median eGFR = 49 (40 to 62) mL/min/1.73m2) participated in this IRB approved study. MRI data were acquired using 3T scanner. Following baseline MRI, each individual received 20 mg furosemide iv, and BOLD MRI scans repeated. R2* was used as BOLD MRI parameter, higher values of which indicate lower tissue oxygenation. Lower values of apparent diffusion coefficient (ADC) suggest higher levels of fibrosis. Annual loss of renal function (eGFR_slope) was estimated using eGFR measurements obtained from electronic medical records over a period of 2-7 years. MRI data and their associations with baseline eGFR, eGFR_slope were analyzed using Spearman correlation and linear regression analyses using SPSS.


R2* was not associated with eGFR or eGFR_slope. Medullary response to furosemide (ΔR2*_Medulla) (ρ = 0.401, p= 0.014) and cortical perfusion (ρ= 0.441, p = 0.009) showed positive association with annual loss of eGFR. Cortical ADC was associated with cortical perfusion; but not with eGFR or eGFR_slope. The association for ΔR2*_Medulla (but not the cortical perfusion) vs. eGFR_slope remained significant even after adjusting for baseline eGFR, age, BMI, gender, systolic blood pressure and blood glucose. In those individuals (n=9) with > 3 ml/min annual loss of eGFR, ΔR2*_Medulla (1.90 ± 2.53 vs. 5.39 ± 3.65 s-1; p = 0.007) and cortical perfusion (88.99 ± 30.31 vs. 117.11 ± 34.76 ml/min/100gm; p = 0.045) were lower compared to the rest.


Quantitative functional MRI measurements may be useful in identifying individuals with moderate but progressive CKD. Larger prospective studies should be performed to confirm these associations.


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