What causes diminished corticomedullary differentiation in renal insufficiency?

Abstract

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 99m Tc-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 Ϯ 176.0 msec (mean Ϯ standard deviation [SD]). Regression analysis showed a negative correlation between cortex T1 and SKGFR (r ϭ -0.5; P ϭ 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 ϭ 0.58; P Ͻ 0.01). In all five kidneys with a corticomedullary contrast-to-noise ratio (CNR) Ͻ5.0 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. ON T1-WEIGHTED MR IMAGES of the normal healthy kidney, the cortex can be clearly differentiated from the medulla, a characteristic referred to as corticomedullary differentiation (CMD). CMD reflects the T1 differences between the cortex and medulla, where the cortex, due to its shorter T1 relaxation time, appears hyperintense with respect to the medulla. Loss of CMD has been observed in renal insufficiency, secondary to a variety of etiologies, including glomerulonephritis, acute tubular necrosis, end-stage chronic renal failure, obstructive hydronephrosis, Fabry's disease, and acute allograft rejection (1-8). While average T1 values in normal adult kidneys at 1.5 T have been reported to be 882 Ϯ 59 msec (mean Ϯ standard deviation [SD]) for cortex and 1163 Ϯ 118 msec for medulla (9), to our knowledge, the underlying changes in T1 at 1.5 T that result in loss of CMD in renal insufficiency have not been determined. Our purpose was to investigate whether the loss of CMD is attributable to changes in T1 values of the cortex, medulla, or both. MATERIALS AND METHODS PatientsThis study included a total of 10 patients (five female, five male) ranging from 38 to 90 years of age (69.8 Ϯ 16.9 years) who were referred for suspected renovascular disease. Patients had underlying diagnoses of chronic renal failure and hypertension (N ϭ 1) and hypertension alone (N ϭ 9) and were being evaluated for renal artery stenosis. Serum creatinine levels in five patients were less than 1.0 mg/dL (range ϭ 0...

Pseudonormal Corticomedullary Differentiation of the Kidney Assessed on T₁-weighted Imaging for Chronic Kidney Disease Patients with Cirrhosis

“…In the normal kidney, corticomedullary differentiation (CMD) is clearly visualized on T 1 -weighted images. [2][3][4][5][6][7][8][9] CMD reflects the differences in T 1 values between the cortex and medulla; with a shorter T 1 relaxation time, the cortex appears hyperintense compared with the medulla. 2 Loss of CMD is observed in renal insufficiency induced by a variety of etiologies, including glomerulonephritis, acute tubular necrosis, end-stage chronic renal failure, obstructive hydronephrosis, and acute allograft rejection.…”

“…2 Loss of CMD is observed in renal insufficiency induced by a variety of etiologies, including glomerulonephritis, acute tubular necrosis, end-stage chronic renal failure, obstructive hydronephrosis, and acute allograft rejection. [2][3][4][5][6][7][8][9] In patients with renal insufficiency, reduced CMD is primarily attributable to an increase in the T 1 value of the cortex. 8 Thus, in daily practice, T 1 -weighted imaging is useful for identifying renal insufficiency because the estimated glomerular filtration rate (eGFR), the clinical marker of renal function, depends largely on patient gender, hydration status, and exercise level.…”

“…[2][3][4][5][6][7][8][9] In patients with renal insufficiency, reduced CMD is primarily attributable to an increase in the T 1 value of the cortex. 8 Thus, in daily practice, T 1 -weighted imaging is useful for identifying renal insufficiency because the estimated glomerular filtration rate (eGFR), the clinical marker of renal function, depends largely on patient gender, hydration status, and exercise level. 8 Recently, Lee and associates described an increase in CMD of the kidneys in patients with cirrhosis with normal renal function compared with Magn Reson Med Sci, Vol.…”

Renovascular imaging in the NSF Era

“…Kidneys with Cyclosporin A toxicity demonstrate normal CMD. In a study by Lee et al, the loss of CMD is ascribed to an increase in the cortex T1 (58).…”

Renal Corticomedullary Differentiation by Non-contrast-enhanced MR Imaging with a Spatially Selective IR Pulse at Various Inversion Times: Comparison with Fast Asymmetric Spin Echo (FASE) and Steady-state Free-precession (SSFP)

“…However, in patients with renal insufficiency, loss of corticomedullary differentiation in non-contrastenhanced MR imaging 2,3 has prevented proper measurement of renal cortical thickness or volume.…”