Acute tubular necrosis (ATN) is the most frequent cause of acute kidney injury. It most often results from taking medications that can injure the kidneys, an insufficient blood supply to the kidneys, or sepsis.

Symptoms may include low urine output and tiredness.

A urinalysis and various blood tests can help differentiate the condition from other kidney disorders.

Doctors may use diuretics — drugs that cause increased urination — to manage fluid overload. However, they do not treat the condition. Hemodialysis may be necessary when diuretics are not effective.

Keep reading to learn more about acute tubular necrosis, including symptoms, causes, risk factors, tests, treatment, and outlook.

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Acute tubular necrosis, or ATN, is the most common intrinsic or renal cause of acute kidney injury. A history of low blood pressure, dehydration, or exposure to nephrotoxic drugs can lead to ATN. Nephrotoxic drugs can cause damage to the kidneys.

The name of the disease implies that it involves the death of kidney tubular epithelial cells, which are an outer layer of cells in the tubules. Kidney tubules return filtered nutrients that the body needs back into the bloodstream.

However, acute tubular necrosis is a misnomer because the death of cells in the tubules is usually minimal. Also, the condition involves more of the kidneys than the tubules.

Acute kidney necrosis manifests most frequently in people who are in the hospital. It can happen in response to the following:

  • exposure to toxins
  • ischemia, an insufficient blood supply to the kidney
  • sepsis, an extreme response to an infection

Generally, people with this condition may experience the following:

Sepsis due to infection is a potentially life threatening condition that can lead to ATN.

Some common symptoms of sepsis include:

  • fever or cold temperature
  • confusion or disorientation
  • shortness of breath
  • fast heart rate

The causes can be divided into the following:


The kidneys metabolize and eliminate many medications. Some of these medications act as toxins that can injure the kidneys and lead to acute tubular necrosis. Such medications include:

  • sulfa drugs, such as sulfamethoxazole-trimethoprim (Bactrim)
  • some antibiotics given intravenously, such as vancomycin (Firvanq) and aminoglycosides (Garamycin)
  • antifungals, such as amphotericin B (Fungizone)
  • antivirals, such as acyclovir (Zovirax) and foscarnet (Foscavir)
  • chemotherapy medications, such as cisplatin (Platinol) and everolimus (Afinitor)
  • contrast dyes used with CT scans, angiograms, or similar procedures
  • drugs that suppress the immune system, such as cyclosporine (Neoral)


An array of conditions can lead to ischemic-induced acute tubular necrosis. Common ones include the loss of body fluid through:

Liver cirrhosis or severe liver dysfunction may lead to inadequate blood flow to the kidney. Also, in congestive heart failure, the heart is unable to pump blood to the body tissues, including the kidney. These can lead to ATN.

Other ischemic causes include:

  • anaphylaxis, a severe allergic reaction that can dilate blood vessels throughout the body
  • conditions involving abnormal blood clotting
  • conditions involving excessive bleeding


Sepsis may induce low blood pressure and reduced blood flow to the kidneys. Both of which lead to kidney damage and may cause ATN.

Risk factors for ATN may include:

The following tests can help differentiate acute tubular necrosis from other causes of acute kidney injury:

  • Serial measurements of kidney function or creatinine: Creatinine is a waste product that the body produces. If kidney disease becomes advanced, then levels of creatinine in the blood rise.
  • Urine sodium concentration: This refers to the amount of sodium, or salt, in a person’s urine. Values higher than 40–50 milliequivalents per liter indicate a diagnosis.
  • Fractional excretion of sodium: This refers to the amount of sodium that has left the body via urine compared to the amount that the kidneys filters and reabsorb. Doctors calculate this value. However, it is not always accurate in people with certain conditions.
  • Urine microscopy: This test assesses a person’s urine for signs of acute tubular necrosis. The urine may have cells within in that appear as “muddy brown casts”. This can indicate that renal tubular epithelial cells have sloughed off.

Doctors may use diuretics to manage urine volume but not to treat the condition. Other supportive treatments may include:

  • managing fluid intake
  • discontinuing nephrotoxic drugs
  • treating infection, avoiding nephrotoxic drugs where possible
  • nutritional support

If diuretics do not manage fluid overload, hemodialysis may be necessary. Critically ill people may need continuous, or 24/7, hemodialysis. A hemodialysis machine filters fluids, wastes, and salts from the blood, when the kidney is unable to function as it should.

Learn more about hemodialysis and the effect it can have on a person.

The death rate depends on the underlying condition.

Factors that result in a poorer outlook include:

Some interventions that may decrease the risk of acute tubular necrosis in high risk populations include:

  • maintaining fluid volume in the body
  • maintaining moderate blood pressure
  • avoiding nephrotoxic drugs, such as NSAIDs and certain antibiotics, if possible

Some complications that can occur in people with acute tubular necrosis are the following:

  • electrolyte disturbances, such as
    • hyperkalemia, or high potassium levels
    • hypocalcemia, or low calcium levels
    • hyperphosphatemia, or high phosphorus levels
  • volume overload, from producing too little urine
  • adverse effects from having high levels of urine in the blood, such as:
    • increased tendency to blood
    • swelling of the sac-like tissue that surrounds the heart
    • altered mental state

Learn more about electrolyte imbalance and how it affects the body.

Acute tubular necrosis usually manifests in people who are in the hospital.

Causes may include the toxic effects of certain medications and insufficient blood supply to the kidneys from conditions, such as diarrhea and vomiting. Sepsis may also play a role.

If the condition stems from reduced blood volume, symptoms may include dry mucous membranes and a fast heart rate. Complications can entail electrolyte disturbances and an altered mental state.

Diagnosis involves blood tests and a urinalysis, which will show muddy brown cells if the condition is present. Doctors may manage fluid overload with diuretics. However, hemodialysis may be necessary.