Acute Tubular Necrosis
(See also Overview of Kidney Filtering Disorders.)
Acute tubular necrosis is kidney injury caused by damage to the kidney tubule cells (kidney cells that reabsorb fluid and minerals from urine as it forms).
Common causes are low blood flow to the kidneys (such as caused by low blood pressure), drugs that damage the kidneys, and severe bodywide infections.
People have no symptoms unless kidney injury is severe.
Diagnosis is based mainly on the results of laboratory tests.
Treatment is directed at the cause, for example, stopping drugs that are damaging the kidneys, giving intravenous fluids to raise blood pressure, and giving antibiotics to treat infection.
Injury to the kidney tubule cells harms the ability of the kidneys to filter the blood. Thus, waste products such as urea and creatinine build up in the bloodstream.
Acute tubular necrosis usually develops only in people who are seriously ill and in the hospital. The most common causes are
The most common causes of low blood pressure leading to acute tubular necrosis are significant blood loss (due to injury or major surgery), serious burns, serious bodywide infection (sepsis), and pancreatitis.
Sepsis also can directly damage kidney cells, which worsens the effects of the low blood pressure caused by sepsis.
Drugs that commonly damage the kidneys include aminoglycoside antibiotics (such as gentamicin and tobramycin), amphotericin B (a drug used to treat severe, bodywide fungal infections), colistimethate (an antibiotic used to treat infections that develop in people hospitalized for another disorder), vancomycin (an antibiotic used to treat infections that are resistant to other antibiotics and that can cause kidney damage when given in high doses for longer than 2 weeks), and nonsteroidal anti-inflammatory drugs (NSAIDs). Aminoglycosides are more likely to be a cause among people who are older, have had major surgery, or have severe disorders of the liver, gallbladder, or bile ducts. Rarely, exposure to a contrast agent during an imaging procedure can cause kidney damage (contrast nephropathy).
Acute tubular necrosis is more likely to develop in people who are older, are critically ill, or have underlying kidney disorders, diabetes, or both.
People with acute tubular necrosis usually have no symptoms. However, if the condition is severe, kidney failure (loss of most kidney function) develops and people's urine output drops below normal. If kidney failure becomes severe, people may have nausea and vomiting, become weak, develop involuntary muscle spasms, and become confused.
Doctors usually first suspect the disorder when blood tests show signs of kidney injury in people who have been exposed to a possible trigger, such as major surgery, an episode of low blood pressure, or a drug that can damage the kidneys. Similar findings can occur in people who are dehydrated, so doctors use other blood tests and urine tests to diagnose acute tubular necrosis.
Outcome depends on correction of the disorder that caused acute tubular necrosis. If that disorder responds rapidly to treatment, kidney function usually returns to normal in 1 to 3 weeks. Prognosis is usually better if people's urine volume exceeds 400 mL (about 13.5 ounces) every 24 hours. People who are more seriously ill, especially those who require care in an intensive care unit, have a higher risk of death.
Drugs that are damaging to the kidneys are stopped. Doctors also give intravenous fluids as needed to maintain a normal blood flow to the kidneys. Infections and other underlying disorders are treated. Dialysis may be required for patients who do not respond to supportive care.
When a person is very ill, doctors give intravenous fluids and sometimes drugs to maintain blood pressure to try to maintain normal blood flow to the kidneys. Drugs that are damaging to the kidneys are avoided whenever possible. If such drugs are necessary, kidney function is closely monitored. In people with diabetes, blood sugar levels are controlled.