Acute tubular necrosis, also known as acute tubulointerstitial nephritis, accounts for about 75% of all cases of acute renal failure and is the most common cause of acute renal failure in hospitalized patients. Acute tubular necrosis 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 acute tubular necrosis have a better prognosis.
Acute tubular necrosis results from ischemic or nephrotoxic injury, most commonly in debilitated patients, such as the critically ill or those who have undergone extensive surgery.
· Severe hypotension
· Heart failure
· Transfusion reactions
· Certain medications
· Contrast media
When ischemic injury occurs, the tubular cells of the kidney suffer from cellular energy depletion, intracellular accumulation of calcium, and damage to the cell membranes. Patch necrosis results at multiple points in the tubules, the basement membrane may be ruptured, and the tubular lumen may become occluded by casts and debris. If the episode of acute tubular necrosis isn't fatal, regeneration eventually will completely reverse the damage.
When nephrotoxic injury occurs, hemoglobin or myoglobin precipitates in the urine. Tubular cells are destroyed by direct toxic effects, lysis of red blood cells (RBCs), intravascular coagulation, occlusion of tubules, and tissue hypoxia. In this form of acute tubular necrosis, most necrosis occurs in the proximal tubules.
Signs and symptoms
· Early stages: effects of primary disease may mask symptoms of acute tubular necrosis
· Decreased urine output may be first recognizable effect
· Uremic syndrome, with oliguria (or, rarely, anuria) and confusion, which may progress to uremic coma
· Heart failure, uremic pericarditis
· Pulmonary edema, uremic lung
· Intractable vomiting
· Poor wound healing
Fever and chills may signal the onset of an infection, the leading cause of death in acute tubular necrosis.
Diagnostic test results
· Urine analysis shows sediment containing RBCs and casts, low specific gravity (1.010), osmolality less than 400 mOsm/kg, and high sodium level (40 to 60 mEq/L).
· Blood studies reveal elevated blood urea nitrogen and creatinine levels, anemia, defects in platelet adherence, metabolic acidosis, and hyperkalemia.
· Electrocardiogram shows arrhythmias and, with hyperkalemia, widening QRS segment, disappearing P waves, and tall, peaked T waves.
· Vigorous supportive measures until normal kidney function resumes; initial treatment may include:
§ I.V. fluids to flush tubules of cellular casts and debris and to replace fluid loss
Long-term fluid management
· Daily replacement of projected and calculated losses (including insensible loss)
Other measures to control complications
· Epoetin alfa to stimulate RBC production; packed RBCs for anemia
· Antibiotics for infection
· Emergency I.V. administration of 50% glucose, regular insulin, and sodium bicarbonate for hyperkalemia
· Sodium polystyrene sulfonate with sorbitol by mouth or by enema to reduce extracellular potassium levels
· Continuous renal replacement therapies