The loss of CMD has been associated with renal insufficiency secondary to a variety of etiologies. Our study shows that this loss of CMD is due primarily to an increased T1 relaxation time of the cortex.
On T1-weighted MR images of the normal healthy kidney, the signal intensity of renal cortex is typically higher than medulla, resulting in
easily visualized corticomedullary differentiation (CMD). Loss of CMD has been observed in renal insufficiency secondary to a variety of etiologies,
such as glomerulonephritis, acute tubular necrosis, end-stage chronic renal failure, obstructive hydronephrosis, and acute allograft rejection (1-3).
While average T1 values for the cortex and medulla in normal kidneys have been reported (882 ± 59 msec and 1163 ± 118 msec, respectively, at
1.5T, for example (4)), to our knowledge, the underlying changes in T1 that result in loss of CMD in renal insufficiency have not been reported. Our
purpose was to investigate whether the loss of CMD associated with decreasing renal function (as measured by single kidney glomerular infiltration
rate (SKGFR)) is attributable to changes in T1 values of the cortex, medulla, or both.
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