Acute Tubular Necrosis
Alternative names :- Necrosis - renal tubular; ATN; Necrosis - acute tubular
Also known as acute tubulointerstitial nephritis, acute tubular necrosis (ATN) accounts for about 75% of all cases of acute renal failure. Its the most common cause of acute renal failure in critically ill patients. ATN injures the tubular segment of the nephron, causing renal failure and uremic syndrome. Mortality ranges from 40% to 70%, depending on complications from underlying diseases. Nonoliguric forms of ATN have a better prognosis.
ATN results from ischemic or nephrotoxic injury, most commonly in debilitated patients, such as the critically ill and those who have undergone extensive surgery.
In ischemic injury, disruption of blood flow to the kidneys may result from circulatory collapse, severe hypotension, trauma, hemorrhage, dehydration, cardiogenic or septic shock, surgery, anesthetics, or reactions to transfusions. Ischemic ATN can damage the epithelial and basement membranes and can cause lesions in the renal interstitium.
In nephrotoxic injury, damage may follow ingestion of certain chemical agents or result from a hypersensitive reaction of the kidneys. Because nephrotoxic ATN doesn't damage the basement membrane of the nephron, it's potentially reversible.
ATN may result from:
Signs and symptoms
ATN is usually difficult to recognize in its early stages because effects of the critically ill patient's primary disease may mask the symptoms of ATN. The first recognizable effect may be decreased urine output. Generally, hyperkalemia and the characteristic uremic syndrome soon follow, with oliguria (or, rarely, anuria) and confusion, which may progress to uremic coma. Other possible complications include heart failure, uremic pericarditis, pulmonary edema, uremic lung, anemia, anorexia, intractable vomiting, and poor wound healing due to debilitation.Fever and chills are ominous signs of infection, the leading cause of death in ATN.
ATN is hard to diagnose accurately until it has progressed to an advanced stage. The most significant laboratory clues are urinary sediment containing RBCs and casts and diluted urine with a low specific gravity (1.010), low osmolality « 400 mOsmlkg), and high sodium level (40 to 60 mEq/L).Blood studies reveal elevated blood urea nitrogen and serum creatinine levels, anemia, defects in platelet adherence, metabolic acidosis, and hyperkalemia. An electrocardiogram may show arrhythmias (from electrolyte imbalances) and, with hyperkalemia, a widening QRS segment, disappearing P waves, and tall, peaked T waves
Vigorous supportive measures are required during the acute phase of ATN until normal kidney 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. However, this treatment carries a risk of fluid overload. Longterm 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. Hyperkalemia may require emergency I. V. administration of 50% glucose, regular insulin, and sodium bicarbonate. Sodium polystyrene sulfonate with sorbitol may be given orally or by enema to reduce extracellular potassium levels. Peritoneal dialysis or hemodialysis may be needed if the patient is catabolic.
The duration of symptoms of ATN is variable. The decreased urine output phase may last from a few days to 6 weeks or more. This is occasionally followed by a period of high urine output, where the healed and newly refunctioning kidneys attempt to clear the body of fluid and wastes. One or two days after urine output rises, symptoms reduce and laboratory values begin to return to normal.
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