Acute tubular necrosis (ATN) is caused by ischemia of the kidneys (lack of oxygen to the tissues), or by exposure to materials that are poisonous to the kidney (nephrotoxic agents).

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 associated with the development of acute renal failure.

ATN, along with prerenal azotemia are the most common causes of renal failure in hospitalized patients. Risks for acute tubular necrosis include injury or trauma with resulting damage to the muscles, recent major surgery, blood transfusion reaction, septic shock or other forms of shock, and severe hypotension (low blood pressure) that lasts longer than 30 minutes.

Any condition that causes a reduction in the amount of blood being pumped by the heart may cause ATN. Liver disease and damage caused by diabetes mellitus (diabetic nephropathy) may make a person more susceptible to the condition.

ATN can be caused by:

• Exposure to nephrotoxic agents such as aminoglycoside antibiotics
• Antifungal agents such as amphotericin
• Medications to prevent rejection of transplanted organs such as cyclosporine
• Dye used for radiographic (x-ray) studies

• Urine output, decreased or none
• Urination, excessive volume
• Urination, excessive at night
• Generalized swelling, fluid retention
• Nausea, vomiting
• Decreased consciousness
  • Drowsy, lethargic, hard to arouse
  • Delirium or confusion
  • Coma
• Seizures
• Easy bruising or bleeding
• Vomiting blood
• Bloody stools
• Decrease in sensation, especially the hands or feet
• Chills, shaking
• Abnormal urine color
• Blood in the urine
• Joint pain
• Flank pain

• Urinalysis may show casts, renal tubular cells, and red blood cells.
• Urine sodium may be high.
• Fractional excretion of sodium and of urea may be relatively high.
• Urine specific gravity and osmolarity urine indicate dilute urine.
• The ratio of urine to plasma (blood) levels of creatinine and urea may be reduced.
• BUN and serum creatinine levels may increase.

• RBC; urine
• Potassium; urine
• Osmolality
• Creatinine clearance
• Creatinine - urine
• Abdominal MRI

In most people, acute tubular necrosis is a reversible lesion. The goal of treatment is to prevent life-threatening complications of acute renal failure during the time the lesion is present.

Treatment focuses on preventing the excess accumulation of fluids and wastes while allowing the kidneys to heal. Observation for deterioration of kidney function should be ongoing.

Fluid intake may be restricted to a volume equal to the volume of urine produced.

The intake of substances that are normally excreted by the kidney may be restricted to minimize their buildup in the body. This may include a diet high in carbohydrates, low in protein, reduced sodium, and reduced potassium.

The underlying cause must be identified and treated.

Diuretics may be used to increase the excretion of fluid from the kidney. Medications may be given to control potassium levels in the bloodstream.

Dialysis may be used to remove excess waste and fluids. This often makes the person feel better, and may make the kidney failure easier to control. Dialysis may not be necessary for all people, but is frequently lifesaving, particularly if serum potassium is dangerously high.

Decreased mental status, pericarditis, increased potassium levels, total lack of urine production, fluid overload, and uncontrolled accumulation of nitrogen waste products are common indications for dialysis.

• Increased risk of infection
• Gastrointestinal loss of blood
• Chronic renal failure
• End-stage renal disease
• Hypertension