URINARY TRACT OBSTRUCTION

Pathophysiology of urinary tract obstruction
Effects of obstruction on renal blood flow and ureteric pressure
Acute unilateral obstruction of a ureter (UUO)
Leads to a triphasic relationship between renal blood flow (RBF) and ureteric pressure.
- Phase 1 (up to 1.5h post obstruction): ureteric pressure rises, RBF rises (afferent arteriole dilatation).
- Phase 2 (from 1.5 5h post obstruction): ureteric pressure continues to rise, RBF falls (efferent arteriole vasoconstriction).
- Phase 3 (beyond 5h): ureteric pressure falls, RBF continues to fall (afferent arteriole vasoconstriction).

Acute bilateral obstruction of a ureter (BUO) or obstruction of a solitary kidney
- Phase 1 (up to 1.5h post obstruction): ureteric pressure rises, RBF rises (afferent arteriole dilatation).
- Phase 2 (from 1.5 5h post obstruction): ureteric pressure continues to rise, RBF is significantly lower than that during unilateral ureteric obstruction.
- Phase 3 (beyond 5h): ureteric pressure remains elevated (in contrast to UUO). By 24 hours RBF has declined to the same level for both unilateral and bilateral ureteric obstruction.

In UUO, the decrease in urine flow through the nephron results in a greater degree of Na absorption, so Na excretion falls. Water loss from the obstructed kidney increases.
Release of BUO is followed by a marked natriuresis, increased K excretion, and a diuresis (a solute diuresis). This is due to:
- an appropriate (physiological) natriuresis, to excrete excessive Na which is a consequence of BUO
- a solute diuresis from the accumulation of urea in extracellular fluid
- a diminution of the corticomedullary concentration gradient, which is normally established by the countercurrent mechanism of the loop of Henle, and is dependent on maintenance of flow through the nephron reduction of flow, as occurs in BUO, reduces the efficiency of the countercurrent mechanism (effectively, the corticomedullary concentration gradient is washed out ).

There may also be accumulation of natriuretic peptides (e.g. ANP) during BUO which contributes to the natriuresis following release of the obstruction.