Editing Pathophysiology of Urinary Tract Obstruction (section)

=== Unilateral ureteral obstruction ===

* '''Triphasic pattern of renal blood flow (RBF) and ureteral pressure changes'''
*# '''First phase'''
*#* '''Initial 1-2 hours'''
*#* '''Increase in pressure within the renal tubules''' '''and a subsequent decrease in GFR'''.
*#* '''To compensate for this decreased GFR, there is an increase in RBF due to afferent arteriolar vasodilation'''
*#** '''Several mechanisms for this increase in RBC have been postulated, including vasodilation from prostaglandins, nitric oxide and tubuloglomerular feedback.'''
*#*** '''Administration of either a prostaglandin synthesis inhibitor (NSAID) or a nitric oxide synthase inhibitor has been shown to block the vasodilatory response and should therefore be avoided in the context of urinary obstruction.'''
*#*** '''ACE-inhibitors or angiotensin receptor blockers reduce constriction at the efferent and affarent arteriole, with a stronger effect on efferent.'''

**# '''Second phase'''
**#* '''From 2-5 hours'''
**#* '''Ureteral[/tubular] pressure remains elevated but RBF begins to decline. As a result, GFR declines'''
**#** '''The decline in GFR is accompanied by an increase in efferent arteriole resistance'''
**#*** '''Activation of the renin-angiotensin system appears to play a role in the efferent arteriole vasoconstriction''' along with endothelin and thromboxane A2.
**#** Note that SASP 2017 suggests that efferent arteriole constriction does not occur in the second phase of UUO, only the second phase of BUO. However, 2015 AUA Update on post-obstructive diuresis suggests that efferent arteriole constriction occurs in the second phase of both UUO and BUO.
**# '''Third phase'''
**#* '''Both ureteral[/tubular] pressure and RBF flow progressively decline, resulting in a gradual loss in renal function'''
**#* '''By about 24 hours after obstruction, the pressure has declined to pre-occlusion levels or even less.''' GFR remains decreased compared to baseline.
**#** '''In addition, there is a shift of blood flow from the outer to inner cortex with UUO that is opposite to that which is seen with BUO.'''
** Renin-mediated hypertension sometimes occurs in acute unilateral renal obstruction and may present a clinical picture suggestive of a renovascular etiology; however, angiographic studies can distinguish if the hypertension is due to a vascular lesion.