Abstract

Renal colic is one of the most common diagnoses of emergency room access and ureteral stone is one of the most common causes of renal colic due to ureteral obstruction. Ureteral obstruction initially causes an increase of intraureteral pressure, which returns to baseline values after a short time after the reduction in urine production and the progressive increase in the circumference and ureter length. Reduction in urinary flow depends on the renal hemodynamic response, which has three phases: initial vasodilation of the preglomerular afferent artery; vasoconstriction of the postglomerular efferent artery; and, finally, vasoconstriction of the preglomerular afferent artery. Renal parenchyma ischemia is associated with oxidative stress, inflammatory infiltrate and subsequent apoptosis of tubular cells and interstitial fibrosis. This degenerative pathological process tends to continue even after relatively early removal of the obstruction and despite the restoration of renal hemodynamics. Fibrosis progression is associated with alterations in renal function with hyperfiltration in the surviving nephronic population and alterations in tubular function. These pathophysiological aspects have to be considered in the management of patients with renal colic and ureteral obstruction. Expulsive treatment of renal stones should be carefully planned by accurate selection of patients and frequent follow-up controls. When the obstruction is severe or the expulsion time is prolonged, early treatment or temporary urinary diversion with deferred treatment should be considered. The time limit for awaiting spontaneous stone passage is not well defined and varies depending on the degree of obstruction and possible complicating factors, however it may be prudent to not exceed two to three weeks.

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