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Acute tubular necrosis

Necrosis - renal tubular; ATN; Necrosis - acute tubular

 

Acute tubular necrosis is a kidney disorder involving damage to the tubule cells of the kidneys, which can lead to acute kidney failure .

Causes

 

Acute tubular necrosis (ATN) is often caused by a lack of blood flow and oxygen to the kidney tissues (ischemia of the kidneys). It may also occur if the kidney cells are damaged by a poison or harmful substance.

The internal structures of the kidney, particularly the tissues of the kidney tubule, become damaged or destroyed. ATN is one of the most common structural changes that can lead to acute renal failure.

ATN is a common cause of kidney failure in hospitalized people. Risks for ATN include:

  • Blood transfusion reaction
  • Injury or trauma that damages the muscles
  • Low blood pressure (hypotension) that lasts longer than 30 minutes
  • Recent major surgery
  • Septic shock due to severe infection

Liver disease and kidney damage caused by diabetes ( diabetic nephropathy ) may make a person more susceptible to the condition.

ATN can also be caused by:

  • Dye (contrast) used for x-ray (radiology) studies
  • Medicines that are toxic to the kidneys (such as aminoglycoside antibiotics or amphotericin)

 

Symptoms

 

Symptoms may include any of the following:

  • Decreased consciousness , coma, delirium or confusion , drowsiness, and lethargy
  • Decreased urine output or no urine output
  • General swelling, fluid retention
  • Nausea, vomiting

 

Exams and Tests

 

The health care provider will perform a physical exam. The provider may hear abnormal sounds when listening to the heart and lungs with a stethoscope ( auscultation ). This is due to too much fluid in the body.

Tests that may be done include:

  • BUN and serum creatinine
  • Fractional excretion of sodium
  • Kidney biopsy
  • Urinalysis
  • Urine sodium
  • Urine specific gravity and osmolarity urine

 

Treatment

 

In most people, ATN is reversible. The goal of treatment is to prevent life-threatening complications of acute kidney failure

Treatment focuses on preventing the buildup of fluids and wastes, while allowing the kidneys to heal.

Treatment may include any of the following:

  • Identifying and treating the underlying cause of the problem
  • Restricting fluid intake
  • Taking medicines to help control potassium level in the blood
  • Medicines taken by mouth or through an IV to help remove fluid from the body

Temporary dialysis can remove excess waste and fluids. This can help improve your symptoms so that you feel better. It may also make kidney failure easier to control. Dialysis may not be necessary for all people, but is often lifesaving, especially if potassium is dangerously high.

Dialysis may be needed in the following cases:

  • Decreased mental status
  • Fluid overload
  • Increased potassium level
  • Pericarditis
  • Removal of toxins that are dangerous to the kidneys
  • Total lack of urine production
  • Uncontrolled buildup of nitrogen waste products

 

Outlook (Prognosis)

 

ATN can last for a few days to 6 weeks or more. This may be followed by 1 or 2 days of making an unusually large amount of urine as the kidneys recover. Kidney function often returns to normal, but there may be other serious problems and complications.

 

When to Contact a Medical Professional

 

Call your provider if your urine output decreases or stops, or if you develop other symptoms of ATN.

 

Prevention

 

Promptly treating conditions that can lead to decreased blood flow as well as decreased oxygen to the kidneys can reduce the risk for ATN.

Blood transfusions are crossmatched to reduce the risk of incompatibility reactions.

Diabetes, liver disorders, and heart problems need to be managed well to reduce the risk for ATN.

If you know you're taking medicine that can injure your kidneys, ask your provider about having your blood level of the medicine checked regularly.

Drink a lot of fluids after having any contrast dyes to allow them to be removed from the body and reduce the risk for kidney damage.

 

 

Open References

References

Molitoris BA, Sharfuddin A. Pathophysiology of acute kidney injury. In: Alpern RJ, Moe OW, Caplan MJ, eds. Seldin and Giebisch's The Kidney . 5th ed. Philadelphia, PA: Elsevier; 2013:chap 76.

Turner JM, Coca SG. Acute tubular injury and acute tubular necrosis. In: Gilbert SJ, Weiner DE, eds. National Kidney Foundation Primer on Kidney Diseases . 6th ed. Philadelphia, PA: Elsevier Saunders; 2014:chap 34.

 
  • Kidney anatomy

    Kidney anatomy - illustration

    The kidneys are responsible for removing wastes from the body, regulating electrolyte balance and blood pressure, and stimulating red blood cell production.

    Kidney anatomy

    illustration

  • Kidney - blood and urine flow

    Kidney - blood and urine flow - illustration

    This is the typical appearance of the blood vessels (vasculature) and urine flow pattern in the kidney. The blood vessels are shown in red and the urine flow pattern in yellow.

    Kidney - blood and urine flow

    illustration

    • Kidney anatomy

      Kidney anatomy - illustration

      The kidneys are responsible for removing wastes from the body, regulating electrolyte balance and blood pressure, and stimulating red blood cell production.

      Kidney anatomy

      illustration

    • Kidney - blood and urine flow

      Kidney - blood and urine flow - illustration

      This is the typical appearance of the blood vessels (vasculature) and urine flow pattern in the kidney. The blood vessels are shown in red and the urine flow pattern in yellow.

      Kidney - blood and urine flow

      illustration

    A Closer Look

     

      Self Care

       

        Tests for Acute tubular necrosis

         
         

        Review Date: 9/22/2015

        Reviewed By: Charles Silberberg, DO, private practice specializing in nephrology, affiliated with New York Medical College, Division of Nephrology, Valhalla, NY. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Isla Ogilvie, PhD, and the A.D.A.M. Editorial team.

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