In a patient with decreased urine output, it is useful to review the operative and anesthetic record to look for any events that may be contributing to the drop in urine output. For example, in patients who appear to be hypovolemic, checking the record for their estimated intraoperative blood loss, complications during the surgery that can relay possible sites of hemorrhage, administration of anticoagulants, requirement of pressors or blood products, and the amount of fluids received is essential in discovering the etiology.

The most common presentation of AKI is prerenal azotemia. Most patients are asymptomatic and present with only a rise in BUN and creatinine (azotemia). The earliest sign of AKI is oliguria (please see below).

Physical exam signs that are specific for AKI are rare.

The normal urine output for an adult is considered 0.5–1.0 mL/kg/hour. For children, normal urine output is 1.0–2.0 mL/kg/hour. Oliguria describes decreased but not absent urine output and is defined as a urine output less than 0.5 mL/kg/hour for two consecutive hours. When the output becomes less than 50 mL-100 mL of urine over a 24-hour period, the patient is considered to be anuric. Producing absolutely no urine is unusual and may be a result of a technical error (discussed in section Management).

The most common nephrotoxic medications are intravenous contrast agents, aminoglycosides (e.g. gentamicin), amphotericin, cisplatin, cyclosporine, and NSAIDs.

Patients with preexisting renal damage (e.g., glomerulonephritis, diabetes) are at greatest risk. Contrast-induced acute kidney injury is widely defined as an absolute increase in serum creatinine of 0.5 mg/dL or a relative increase of 25 % from the baseline value, assessed 48–72 hours following intravascular administration of contrast media.

High hydrostatic pressure in the glomerular capillary is responsible for ensuring filtration in the nephron tubules. In situations where hydrostatic pressure in Bowman space rises (postrenal AKI), filtering fluid becomes more difficult.

In most cases, this will not lead to renal failure unless the patient has a solitary kidney.

Yes. This is a result of the response of the adrenal cortex and posterior pituitary to stress from surgery leading to fluid loss and shifts. Aldosterone and anti-diuretic hormone (ADH) released in the first 24 hour after surgery are primarily responsible for both salt and water retention (discussed in section Work-Up). Oliguria lasting for more than 24 hours warrants investigation.

Prolonged periods of poor renal perfusion will directly damage the kidneys and lead to acute tubular necrosis (ATN), which will cause oliguria even after normal perfusion has been restored.

Most general anesthetics, commonly the inhaled volatile agents, result in myocardial depression and systemic vasodilation. This in turn can lead to a decrease in cardiac output and end-organ perfusion. In someone with no preexisting medical conditions or comorbidities, patients usually tolerate temporary fluctuations in their blood pressure without considerable change to their renal and cardiovascular function. However, patients with renal disease at baseline are more susceptible to insult resulting in worsening renal function.

The best initial tests are BUN and creatinine. A BUN/Cr ratio > 20:1 with a clear history of hypoperfusion or hypotension is all one needs to diagnose prerenal AKI.