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Acute Tubular Necrosis (ATN)


Frank O'Brien

, MD, Washington University in St. Louis

Reviewed/Revised Jan 2024
Topic Resources

Acute tubular necrosis (ATN) is 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 characterized by acute tubular cell injury and dysfunction. Common causes are hypotension or sepsis that causes renal hypoperfusion and nephrotoxic medications. The condition is asymptomatic unless it causes renal failure. The diagnosis is suspected when azotemia develops after a hypotensive event, severe sepsis, or medication exposure and is distinguished from prerenal azotemia by laboratory testing and response to volume expansion. Treatment is supportive.

Etiology of Acute Tubular Necrosis

Common causes of acute tubular necrosis include the following:

  • Renal hypoperfusion, most often caused by hypotension or sepsis (ischemic ATN; most common, especially in patients in an intensive care unit)

  • Nephrotoxins

  • Major surgery (often due to multiple factors)

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 Etiology references ) increase the risk of aminoglycoside toxicity. Certain combinations of medications (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:

Etiology references

  • 1. Stokes MB: Vancomycin in the kidney—A novel cast nephropathy. J Am Soc Nephrol 28(6):1669-1670, 2017. doi: 10.1681/ASN.2017010091

  • 2. Aniort J, Poyet A, Kemeny J-L, et al: Bile cast nephropathy caused by obstructive cholestasis. Am J Kidney Dis 69(1):143-146, 2017. doi: 10.1053/j.ajkd.2016.08.023

Symptoms and Signs of Acute Tubular Necrosis

Diagnosis of Acute Tubular Necrosis

  • Differentiation from prerenal azotemia, based mainly on laboratory findings and, in the case of blood or fluid loss, response to volume expansion

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 ).


Treatment of Acute Tubular Necrosis

  • Supportive care

Treatment is supportive and includes stopping nephrotoxins whenever possible, maintaining euvolemia, providing nutritional support, and treating infections (preferably with medications 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.

Pearls & Pitfalls

  • Diuretics may help maintain urinary output in patients with ATN but do not alter the course of kidney injury.

Prognosis for Acute Tubular Necrosis

  • Decreased urine volume (eg, anuria, oliguria)

  • Severity of the underlying disorder

  • Severity of coexisting disorders

Cause of death is usually infection or the underlying disorder.

Prognosis reference

  • 1. Chertow GM, Burdick E, Honour M, et al: Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol 16(11):3365-3370, 2005. doi: 10.1681/ASN.2004090740

Prevention of Acute Tubular Necrosis

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.

Key Points

  • Acute tubular necrosis (ATN) can develop after various disorders or triggers decrease renal perfusion or expose the kidneys to toxins.

  • Other than oliguria in severe cases, symptoms do not develop unless and until renal failure develops.

  • Differentiate ATN from prerenal azotemia by the response to volume expansion and by urine and blood chemistry tests and calculations derived from them.

  • Correct the cause of ATN as soon as possible to achieve a good short-term prognosis.

  • Stop nephrotoxins, maintain euvolemia, and treat infection and undernutrition.

Drugs Mentioned In This Article

Drug Name Select Trade
Amphocin, Fungizone
Platinol, Platinol -AQ
Cequa, Gengraf , Neoral, Restasis, Sandimmune, SangCya, Verkazia, Vevye
FIRVANQ, Vancocin, Vancocin Powder, VANCOSOL
Aluvea , BP-50% Urea , BP-K50, Carmol, CEM-Urea, Cerovel, DermacinRx Urea, Epimide-50, Gord Urea, Gordons Urea, Hydro 35 , Hydro 40, Kerafoam, Kerafoam 42, Keralac, Keralac Nailstik, Keratol, Keratol Plus, Kerol, Kerol AD, Kerol ZX, Latrix, Mectalyte, Nutraplus, RE Urea 40, RE Urea 50 , Rea Lo, Remeven, RE-U40, RYNODERM , U40, U-Kera, Ultra Mide 25, Ultralytic-2, Umecta, Umecta Nail Film, URALISS, Uramaxin , Uramaxin GT, Urea, Ureacin-10, Ureacin-20, Urealac , Ureaphil, Uredeb, URE-K , Uremez-40, Ure-Na, Uresol, Utopic, Vanamide, Xurea, X-VIATE
Aridol, BRONCHITOL, Osmitrol , Resectisol
NOTE: This is the Professional Version. CONSUMERS: View Consumer Version
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