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Acute Tubular Necrosis
Overview

Each glomerulus (microscopic "filtering screen") has a tubule that transports urine to the ureters and metabolically alters the urine and its chemicals. Because the tubules are exceedingly metabolically active, they are very dependent on the oxygen that supplies the tubular cells. They are often described as being nearly oxygen starved because they work so hard. Close to 200 liters of fluid is filtered across the glomeruli, and the tubules reabsorb 99% (198 liters) or the fluid in a selective manner.

Acute tubular necrosis (ATN) is the death of tubular cells, which may result when tubular cells do not get enough oxygen (ischemic ATN) or when they have been exposed to a toxic drug or molecule (nephrotoxic ATN). Fortunately, new tubular cells usually replace those that have died. Indeed, the tubular cells of the kidneys undergo a continuous cycle of cell death and renewal, much like the cells of the skin.

Causes

In the hospital setting, ATN is the most common cause of acute renal failure (ARF). Hospital patients often have acute medical problems that limit the oxygen supplied to the tubules or that cause tubular hypoperfusion (decreased blood flow).

Certain medical and surgical situations are associated with a high risk for developing ischemic ATN:

Some medications and clinical materials can cause nephrotoxic ATN:

  • Aminoglycosides (antibacterial antibiotics such as streptomycin and gentamicin)
  • Amphotericin B (antibiotic used to treat some forms of meningitis and systemic fungal infections)
  • Cisplatin (anticancer agent used to treat late-stage ovarian and testicular cancers)
  • Radioisotopic contrast media (agent used in certain imaging studies)

Exposure to certain molecules also may cause nephrotoxic ATN. For example, when a person suffers significant muscle trauma, such as during a crush injury, the muscle enzyme creatinine phosphokinase (CPK) leaks into the blood. Myoglobulin is the protein that leaks into the blood and ultimately causes ATN. Measurement of CPK is a marker of myoglobulin released by muscle cells. If enough CPK spills into the blood and is filtered through the glomeruli, it can damage the tubules, causing nephrotoxic ATN.

Signs and Symptoms

Acute tubular necrosis (ATN) typically does not produce specific signs or symptoms.

Diagnosis

Diagnosis often is supported by a positive history of risk factors. Yet the physician must rule out other reasons for acute renal failure, such as prerenal, postrenal, and renal ARF. Distinguishing ATN from prerenal ARF can be extremely difficult. Urine chemistry and microscopic examination of the urine help to confirm the diagnosis. ATN does not rapidly improve following the administration of large-volume intravenous fluid.

Treatment

Management relies on aggressive treatment of the factors that precipitated ATN. One exception is the treatment of ATN associated with the breakdown of muscle fibers caused by a crush injury. Aggressive, forced diuresis (i.e., an increased excretion of urine) may improve the condition.

Patients at high risk for developing ARF from contrast induced ATN should be treated with intravenous (IV) fluids prior to contrast exposure to prevent the ATN. There has been a recent report suggesting that pretreatment of these patients with a medication called mucomyst may also help to prevent ARF in patients undergoing IV contrast exposure.

Prognosis
Because tubular cells have the capacity to replace themselves, the overall prognosis for ATN is quite good if the cause is corrected. Once the precipitating factor has been treated and removed, ATN usually resolves within 7 to 21 days. On occasion, the kidneys may not completely recover or (rarely) may never recover, despite the resolution of other medical problems. This situation usually indicates that there is preexisting, unidentified renal dysfunction.  

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