Acute kidney injury (AKI) is the sudden decline of kidney function within a 48-hour period. While definitions vary, one widely used criterion is an increase in serum creatinine (Cr) ≥ 0.3 mg/dL within 48 hours or an increase in serum Cr to ≥ 1.5 times baseline (which is presumed or known to have occurred within the prior 7 days), or urine output < 0.5 mL/kg/hour for 6 hours.

The severity of AKI can be classified using the RIFLE criteria (Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease). Risk is classified as increase in serum Cr to 1.5 times baseline or glomerular filtration rate (GFR) decrease > 25% or urine output < 0.5 mL/kg/hour for 6 hours. Injury is classified as serum Cr increase of 2 times baseline or GFR decrease > 50% or urine output < 0.5 mL/kg/hour for 12 hours. Failure is classified as increase in serum Cr 3 times baseline or GFR decrease > 75% or serum Cr ≥ 4 mg/dL and urine output < 0.3 mL/kg/hour, which is classified as oliguria. Loss is described as persistent acute renal failure and equates to complete loss of renal function > 4 weeks and is classified as end-stage kidney disease when it persists > 3 months. 

AKI is characterized by a decreased glomerular filtration rate and retention of serum blood urea nitrogen (BUN), Cr, and other metabolic wastes typically excreted through the kidneys. The condition is normally reversible if rapidly identified and appropriately managed. Patients may appear ill, usually from the underlying etiology of AKI, but may also be fairly asymptomatic or have nonspecific symptoms. Symptoms may include oliguria, change in mental status, weakness, anorexia, flank or abdominal pain, pallor, pruritus, and nausea. Life-threatening complications include hyperkalemia, severe metabolic acidosis, fluid overload, and uremia. 

Prognosis is good, although heavily dependent on etiology, with a majority of patients recovering adequate renal function. 

Etiology is widely variable. Conditions can be divided into prerenal, intrarenal, and postrenal etiologies:

• Prerenal etiologies include conditions that cause low renal blood flow such as sepsis, pancreatitis, congestive heart failure, anaphylaxis, hypovolemia, cirrhosis, and nephrotoxin exposure. May progress to acute tubular necrosis.
• Intrarenal conditions are those that affect kidney parenchyma or vasculature such as malignant hypertension, systemic lupus erythematosus, viral renal infection, sarcoidosis, and leukemia.
• Postrenal conditions are those that cause renal obstruction such as nephrolithiasis, tumors, strictures, and trauma. 

Patients with AKI may be at increased risk for both short- and long-term cardiovascular complications, including heart failure and pulmonary edema. Interactions between kidney and cardiac diseases are classified as cardiorenal syndromes.

Kidney injury that occurs within days after the intravenous (IV) administration of iodinated contrast material is called contrast-associated acute kidney injury.

Many medications have also been implicated as causes of AKI. See Drug Reaction Data below.

Related topic: Chronic kidney disease