Urinary tract obstruction is a frequent occurrence in the hospitalized setting. Thankfully, after relief of the obstruction a vast majority of patients have complete recovery of kidney function. However, a few patients will have marked polyuria (>4-5L per day) after release of bilateral obstruction. This is termed postobstructive diuresis. There are several physiologic and pathologic factors that lead to the development of this condition.
- Excess sodium and water retention
- Accumulation of urea and other non-reabsorbable solutes resulting in an osmotic diuresis.
- Decreased tubular reabsorption of sodium secondary to altered expression of proximal and distal sodium transporters.
- Inability to maximally concentrate urine, secondary to a decreased medullary concentrating gradient, leading to decreased response to ADH
- Increased tubular transit flow time reducing equilibration time for absorption of sodium and water.
- Increased production of prostaglandins immediately following relief of obstruction.
Patients who develop post obstructive diuresis need to be monitored closely. Especially if the patient is unable to eat and drink on their own. Once the accumulated excess of sodium and water has been excreted, severe volume contraction and hypokalemia can occur. It is important to monitor urine output closely in this setting. Once the patient has diuresed to the point of euvolemia, fluid replacement should be administered as needed to prevent volume contraction. This is done by replacing 75% of the urine losses with 0.45% NS. This condition is usually self-limiting and resolves over several days to a week. Persistent polyuria beyond a week is often due to overzealous volume repletion.