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:

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

  1. Arant B (1987). "Postnatal development of renal function during the first year of life". Pediatr Nephrol. 1 (3): 308–13. PMID 3153294.



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