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Updated: Jul 16, 2026

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
What causes diminished corticomedullary differentiation in renal insufficiency?
Vivian S Lee1, Manmeen Kaur, Louisa Bokacheva
1Department of Radiology, New York University School of Medicine, New York, New York 10016, USA. vivian.lee@med.nyu.edu
Purpose:
To investigate whether the loss of corticomedullary differentiation (CMD) on T1-weighted MR images due to renal insufficiency can be attributed to changes in T1 values of the cortex, medulla, or both.
Materials And Methods:
Study subjects included 10 patients (serum creatinine range 0.6-3.0 mg/dL) referred for suspected renovascular disease who underwent 99mTc-diethylene triamine pentaacetic acid (DTPA) renography to determine single kidney glomerular filtration rate (SKGFR) and same-day MRI, which included T1 measurements and unenhanced T1-weighted gradient echo imaging. Corticomedullary differentiation on T1-weighted images was assessed qualitatively and quantitatively.
Results:
SKGFR values ranged from 3.5 to 89.4 mL/minute based on radionuclide studies. T1 relaxation times of the medulla exceeded those of renal cortex by 147.9+/-176.0 msec (mean+/-standard deviation [SD]). Regression analysis showed a negative correlation between cortex T1 and SKGFR (r=-0.5; P=0.03), whereas there was no significant correlation between medullary T1 and SKGFR. The difference between medullary and cortical T1s correlated significantly with SKGFR (r=0.58; P<0.01). In all five kidneys with a corticomedullary contrast-to-noise ratio (CNR)<5.0 on T1-weighted images, SKGFR was less than 20 mL/minute.
Conclusion:
In our subject population, loss of CMD with decreasing SKGFR can be attributed primarily to an increased T1 relaxation time of the cortex. Medullary T1 values vary but do not appear to correlate with degree of renal insufficiency.
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