Editing Pathophysiology of Urinary Tract Obstruction (section)

==== Causes ====

*'''Will often accompany relief of BUO''' in the presence of a normal contralateral kidney 
**The accumulation of extracellular volume stimulates the synthesis and release of ANP, which promotes increased GFR and sodium excretion. Decreases in the aquaporin water channels in the kidney further promote the diuresis.
**'''COX-2 activity may be increased in the post-obstructive phase and contributes to polyuria, and impaired urine-concentrating ability'''
**One study found that predictors of POD were higher serum creatinine, higher serum bicarbonate and urinary retention.
*'''Not typically observed with relief of UUO''', secondary to the presence of a functional contralateral kidney that can maintain fluid balance
** '''Fractional excretion of sodium after relief of obstruction is greater in BUO than UUO'''
*** The natriuresis following relief of BUO is typically greater than that after UUO
* '''<span style="color:#ff0000">Most patients do not demonstrate a clinically significant POD after relief of urinary tract obstruction</span>'''
**'''<span style="color:#ff0000">Patients at risk for clinically significant POD typically exhibit signs of fluid overload, including (3):</span>'''
**#'''<span style="color:#ff0000">Edema</span>'''
**#'''<span style="color:#ff0000">Congestive heart failure</span>'''
**#'''<span style="color:#ff0000">Hypertension</span>'''
**'''Special consideration should also be given to patients with high urine outputs (>5 to 6 L daily).'''