Decompensation occurs as the ureter lengthens and becomes tortuous, followed by replacement of normal ureteral muscle with scar tissue. As a result, the ureter progressively loses its ability to contract and transport a bolus of urine. In the kidney, pressure from the obstruction is ultimately transmitted to the renal tubules, which leads to reflex vasoconstriction and reduction of renal blood flow. The glomerular filtration rate is thus reduced in the obstructed nephrons. If bilateral, these changes may be associated with acute kidney injury. In chronic, unrelieved obstruction, there may be irreversible atrophic changes in the renal cortex resulting from chronic ischemia and inflammation.
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