Oliguria pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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.
Pathophysiology
The mechanisms causing oliguria can be divided into several categories:
Prerenal
In response to hypoperfusion of the kidney (e.g. as a result of dehydration by poor oral intake, diarrhea, massive bleeding or sepsis)
Renal
Due to kidney damage (severe hypoperfusion, rhabdomyolysis, medication)
Postrenal
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.
Postoperative Oliguria
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 in Infants
Oliguria, when defined as less than 1 mL/kg/h, in infants is not considered to be a reliable sign of renal failure.[1]
References
- ↑ Arant B (1987). "Postnatal development of renal function during the first year of life". Pediatr Nephrol. 1 (3): 308–13. PMID 3153294.