Oliguria pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Oliguria is usually as a result of acute renal insult rather than chronic failure and more commonly due to tubular damage caused by renal hypoperfusion or nephrotoxins, where reabsorption of glomerular filtrate is impaired.

The mechanisms causing oliguria can be divided into several categories:

In response to hypoperfusion of the kidney (e.g. as a result of dehydration by poor oral intake, diarrhea, massive bleeding or sepsis)

Due to kidney damage (severe hypoperfusion, rhabdomyolysis, medication)

As a consequence of obstruction of the urine flow (e.g. enlarged prostate, tumor compression urinary outflow, expanding hematoma or fluid collection)

The decreased production of urine may be a sign of dehydration, renal failure or urinary obstruction/urinary retention.

Patients usually have a decrease in urine output after a major operation that may be a normal physiological response to:

• Fluid/blood loss – decreased glomerular filtration rate secondary to hypovolemia and/or hypotension
• Response of adrenal cortex to stress -increase in aldosterone (Na and water retention) and antidiuretic hormone (ADH) release

Oliguria, when defined as less than 1 mL/kg/h, in infants is not considered to be a reliable sign of renal failure.^[1]

Template:WH Template:WS