Acute Tubular Necrosis

Acute tubular necrosis (also called acute tubulointer­stitial nephritis) is the most common cause of acme renal failure in critically ill patients. It accounts for about 75% of all cases of acute renal failure. This disorder injures the tubular segment of the nephron, causing renal failure and uremic syndrome. mortality can be as high as 70%, depending on complications from underlying diseases. Patients with nonoliguric forms of acute tubular necrosis have a better prognosis.

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:

• Hypotension (low blood pressure)
• Obstetric (birth-related) complications
• Obstructive jaundice
• Prolonged prerenal state
• Sepsis (infection in the blood or tissues)
• Surgery

Signs and Symptoms

• 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.

Diagnostic tests

Diagnosis usually doesn't occur until the condition reaches an advanced stage. The most significant laboratory test findings are urine sediment, containing RBCs and casts, and diluted urine with a low specific gravity (1.010), low osmolality (less than 400 mOsm/kg), and high sodium level (40 to 60 mEq/L).

Blood studies reveal elevated blood urea nitrogen and serum creatinine levels, decreased serum protein levels, anemia, defects in platelet adherence, metabolic acidosis, and hyperkalemia.

An electrocardiogram may show arrhythmias (from electrolyte imbalances). With hyperkalemia, it also may show a widening QRS complex, disappearing P waves, and tall, peaked T waves.

Treatment

Acute tubular necrosis requires vigorous supportive measures during the acute phase until normal renal function resumes. Initial treatment may include administration of diuretics and infusion of a large volume of fluids to flush tubules of cellular casts and debris and to replace fluid loss. This treatment carries a risk of fluid overload. Long-term fluid management requires daily replacement of projected and calculated losses (including insensible loss).

Other appropriate measures to control complications include transfusion of packed RBCs for anemia and administration of antibiotics for infection. A patient with hyperkalemia may require emergency I.V. administration of 50% glucose, regular insulin, and sodium bicarbonate. Sodium polystyrene sulfonate may be given by mouth or by enema to reduce extracellular potassium levels. Peritoneal dialysis or hemodialysis may be needed for a catabolic patient.

Prevention

Prompt treatment of conditions that can result in decreased blood flow and decreased oxygenation of the kidneys may reduce the risk of acute tubular necrosis.

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

Disorders such as diabetes, liver disorders, or cardiac disorders must be controlled as much as possible to reduce the risk of ATN.