Acute kidney injury (AKI) is defined as a rapid decline in renal function characterized by progressive azotemia (clinically measured by serum creatinine and blood urea nitrogen), which may or may not be accompanied by oliguria.

It is important to distinguish the three major causes of AKI: prerenal azotemia, postrenal azotemia or obstruction of the urinary tract, and intrinsic renal disease.

The presence of marked/sudden oliguria or anuria is a powerful diagnostic clue that suggests urinary tract obstruction, severe acute tubular necrosis (ATN) with cortical necrosis, or bilateral vascular occlusion.

If urinary tract obstruction is a diagnostic consideration, renal ultrasonography is sensitive and specific (90% to 95%) in confirming the diagnosis of hydronephrosis.

Diagnostic approach to AKI (see Table 46-6).

The therapy for prerenal azotemia is directed at optimizing volume status with isotonic fluids with the expectant improvement in renal function within 48 hours.

The specific diagnosis of acute interstitial nephritis (AIN) as a cause of acute kidney failure (AKI) should lead to the discontinuation of possibly offending medications. If the renal insufficiency does not resolve in days to weeks, renal biopsy results may confirm the diagnosis of AIN.

The prognosis of ATN is dependent on the underlying primary disease that resulted in AKI as well as any complications that arise during the bout of AKI. The mortality rate for patients with ATN may approach 40% to 50% in certain subgroups.

Data suggest that in azotemic patients who require cardiac angiography, a protocol of intravenous hydration and use of a nonionic contrast material appear warranted. Earlier randomized controlled trials have suggested that pretreatment with acetylcysteine might attenuate contrast injury in at-risk patients; however, more recent reviews have called this putative benefit into question.