Acute tubular necrosis
Acute tubular necrosis is a kidney disorder involving damage to the tubule cells of the kidneys, which can lead to acute kidney failure
.
Alternative Names
Necrosis - renal tubular; ATN; Necrosis - acute tubular
Causes, incidence, and risk factors
Acute tubular necrosis (ATN) is usually caused by a lack of 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 one of the most common causes of kidney failure in hospitalized patients. Risks for acute tubular necrosis include:
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
- Medications that are toxic to the kidneys (such as aminoglycoside antibiotics or amphotericin)
Symptoms
Note: Other symptoms of acute kidney failure may also be present.
Signs and tests
The doctor will perform a physical exam. Your doctor 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.
Other tests that may be done include:
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 excess buildup of fluids and wastes, while allowing the kidneys to heal. Patients should be watched closely for deterioration of kidney function.
Treatment can include:
-
Identifying and treating the underlying cause of the problem
-
Restricting fluid intake to a volume equal to the volume of urine produced
-
Restricting substances normally removed by the kidneys (such as protein, sodium, potassium) to minimize their buildup in the body
-
Taking medications to help control potassium levels in the bloodstream
-
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 make you feel better, and may make the kidney failure easier to control. Dialysis may not be necessary for all people, but is often lifesaving, especially if serum potassium
is dangerously high.
Dialysis may be needed in the following cases:
-
Decreased mental status
-
Fluid overload
-
Increased potassium levels
-
-
To remove toxins that are dangerous to the kidneys
-
Total lack of urine production
-
Uncontrolled buildup of nitrogen waste products
Expectations (prognosis)
How long symptoms last can vary. You may make less urine for a few days to 6 weeks or more. This may be followed by a period of high urine output. This occurs because the healed and newly functioning kidneys try to clear the body of fluid and waste.
One or two days after your urine amount rises, symptoms reduce and test results begin to return to normal.
Complications
- Bleeding from the gastrointestinal tract
- Chronic kidney disease and permanent kidney damage
- High blood pressure
- Increased risk of infection
Calling your health care provider
Call your health care provider if your urine output decreases or stops, or if you develop other symptoms of acute tubular necrosis.
Prevention
Promptly treating conditions that can lead to decreased blood flow as well as decreased oxygen to the kidneys can reduce the risk of acute tubular necrosis.
Blood transfusions are crossmatched to reduce the risk of incompatibility reactions.
Control conditions such as diabetes, liver disorders, and cardiac disorders to reduce the risk of acute tubular necrosis.
Carefully monitor exposure to medications that can be toxic to the kidney. Have your blood levels of these medications checked regularly. Drink a lot of fluids after having any radiocontrast dyes to allow them to be removed from the body and reduce the risk of kidney damage.
References
Clarkson MR, Friedewald JJ, Eustace JA, Rabb H. Acute kidney injury. In: Brenner BM, ed. Brenner and Rector's The Kidney. 8th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 29.
Molitoris BA. Acute kidney injury. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 121.
Updated: 9/20/2011
David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine, Department of Medicine, University of Washington School of Medicine; Herbert Y. Lin, MD, PHD, Nephrologist, Massachusetts General Hospital; Associate Professor of Medicine, Harvard Medical School. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.