[Mechanisms of Postobstructive Polyuria]

Postobstructive diuresis occurs after relief of bilateral ureteral obstruction despite the persistent decrease in renal cortical perfusion and glomerular filtration rate (GFR). After an initial transient rise in renal blood flow (RBF) during acute ureteral obstruction, tubular damage and progressive vasoconstriction with decreased RBF, especially of medullary perfusion, are observed with chronic obstruction. These are associated with an activation of the renin-angiotensin system and of renal prostaglandin (PG) synthesis with enhanced production of the vasoconstrictor thromboxane A2. Azotemia and extracellular fluid volume (ECFV) expansion result from impaired renal function. Mechanisms of polyuria following relief from bilateral chronic obstruction include enhanced PGE-mediated medullary blood flow, structural and functional tubular damage with decreased sodium reabsorption and (vasopressin-resistant) impaired renal concentrating ability, osmotic diuresis, activation of natriuretic factors following ECFV-expansion, and sometimes iatrogenic excessive fluid replacement. The resulting loss of fluid and electrolytes represents a major hazard in patients after surgical correction of congenital or acquired urinary tract obstruction.