Acute Tubular Necrosis (ATN)

Common causes of acute tubular necrosis include the following:

Other causes of ATN include

Common nephrotoxins include the following:

Massive volume loss, particularly in patients with septic or hemorrhagic shock, pancreatitis, or major surgery, increases the risk of ischemic ATN; patients with serious comorbidities are at highest risk.

Major surgery and advanced hepatobiliary disease (2 Etiology references Acute tubular necrosis (ATN) is kidney injury characterized by acute tubular cell injury and dysfunction. Common causes are hypotension or sepsis that causes renal hypoperfusion and nephrotoxic... read more ) increase the risk of aminoglycoside toxicity. Certain drug combinations (eg, aminoglycosides with amphotericin B) may be especially nephrotoxic. NSAIDs may cause several types of intrinsic kidney disease, including ATN.

Toxic exposures cause patchy, segmental, tubular luminal occlusion with casts and cellular debris or segmental tubular necrosis.

Acute tubular necrosis is more likely to develop in patients with the following:

Acute tubular necrosis is usually asymptomatic but may cause symptoms or signs of acute kidney injury, typically oliguria Oliguria Oliguria is urine output < 500 mL in 24 hours in an adult or < 0.5 mL/kg/hour in an adult or child (< 1 mL/kg/hour in neonates). Causes of oliguria are typically divided into 3 categories... read more initially, if ATN is severe. However, urine output may not be reduced if ATN is less severe (eg, typical in aminoglycoside-induced ATN).

Acute tubular necrosis is suspected when serum creatinine rises ≥ 0.3 mg/dL/day (26.5 micromol/liter [μmol/L]) above baseline or a 1.5- to 2.0-fold increase in serum creatinine from baseline after an apparent trigger (eg, hypotensive event, exposure to a nephrotoxin); the rise in creatinine may occur 1 to 2 days after certain exposures (eg, IV radiocontrast) but be more delayed after exposure to other nephrotoxins (eg, aminoglycosides).

ATN must be differentiated from prerenal azotemia because treatment differs. In prerenal azotemia, renal perfusion is decreased enough to elevate serum blood urea nitrogen (BUN) out of proportion to creatinine, but not enough to cause ischemic damage to tubular cells. Prerenal azotemia can be caused by direct intravascular fluid loss (eg, due to hemorrhage, gastrointestinal tract losses, urinary losses) or by a relative decrease in effective circulating volume without loss of total body fluid (eg, in heart failure, portal hypertension with ascites). If fluid loss is the cause, volume expansion using IV normal saline solution increases urine output and normalizes serum creatinine level. If ATN is the cause, IV saline typically causes no increase in urine output and no rapid change in serum creatinine. Untreated prerenal azotemia may progress to ischemic ATN.

Laboratory findings also help distinguish acute tubular necrosis from prerenal azotemia (see table Laboratory Findings Distinguishing Acute Tubular Necrosis From Prerenal Azotemia Laboratory Findings Distinguishing Acute Tubular Necrosis From Prerenal Azotemia ).

In otherwise healthy patients, short-term prognosis is good when the underlying insult is corrected; serum creatinine typically returns to normal or near-normal within 1 to 3 weeks. In sick patients, even when acute kidney injury Acute Kidney Injury (AKI) Acute kidney injury is a rapid decrease in renal function over days to weeks, causing an accumulation of nitrogenous products in the blood (azotemia) with or without reduction in amount of urine... read more is mild, morbidity and mortality are increased. Prognosis is better in patients who do not require treatment in an intensive care unit (32% mortality) than in those who do (72% mortality). Predictors of mortality include mainly

Patients who survive acute tubular necrosis have an increased risk of chronic kidney disease Chronic Kidney Disease Chronic kidney disease (CKD) is long-standing, progressive deterioration of renal function. Symptoms develop slowly and in advanced stages include anorexia, nausea, vomiting, stomatitis, dysgeusia... read more .

Cause of death is usually infection or the underlying disorder.

Treatment is supportive and includes stopping nephrotoxins whenever possible, maintaining euvolemia, providing nutritional support, and treating infections (preferably with drugs that are not nephrotoxic). Diuretics may be used to maintain urine output in oliguric acute tubular necrosis but are of unproven benefit and do not alter the course of kidney injury; there is no evidence to support use of mannitol or dopamine. General management of acute kidney injury Treatment Acute kidney injury is a rapid decrease in renal function over days to weeks, causing an accumulation of nitrogenous products in the blood (azotemia) with or without reduction in amount of urine... read more is discussed elsewhere.

Prevention includes the following:

There is no evidence that loop diuretics, mannitol, or dopamine helps prevent or alter the course of established acute tubular necrosis.