Acute Tubular Necrosis
The most common cause of acute renal failure in critically ill patients, acute tubular necrosis accounts for about 75% of all cases of acute renal failure. Also called acute tubulointerstitial nephritis, 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. Nonoliguric forms of
acute tubular necrosis have a better prognosis.
acute tubular necrosis have a better prognosis.
Causes
Acute tubular necrosis results from ischemic or nephrotoxic injury, most commonly in debilitated patients. In ischemic injury, disrupted blood flow to the kidneys may result from circulatory collapse, severe hypotension, trauma, hemorrhage, dehydration, cardiogenic or septic shock, surgery, anesthetics, or transfusion reactions. Nephrotoxic injury may follow ingestion or inhalation of certain chemicals, such as aminoglycoside antibiotics and radiographic contrast agents, or may result from renal hypersensitivity.
Specifically, acute tubular necrosis can result from any of the following:
diseased tubular epithelium that allows leakage of glomerular filtrate across the membranes and reabsorption of filtrate into the blood
obstructed urine flow from the collection of damaged cells, casts, red blood cells (RBCs), and other cellular debris within the tubular walls
ischemic injury to glomerular epithelial cells, resulting in cellular collapse and decreased glomerular capillary permeability
ischemic injury to vascular endothelium, eventually resulting in cellular swelling, sludging, and tubular obstruction.
Complications
Nephrotoxic acute tubular necrosis doesn’t damage the basement membrane of the nephron, so it’s potentially reversible. However, ischemic acute tubular necrosis can damage the epithelial and basement membranes and can cause lesions in the renal interstitium. Infections (usually septicemia) can complicate up to 70% of all cases and are the leading cause of death. GI hemorrhage, fluid and electrolyte imbalances, and cardiovascular dysfunction may occur during the acute phase or in the recovery phase. Hyperkalemia is the most immediate life-threatening complication. Neurologic complications commonly occur in elderly patients and occasionally in younger ones. Hypercalcemia may occur during the recovery phase.
Assessment
The patient’s history may include an ischemic or nephrotoxic injury that can cause acute tubular necrosis. The signs of acute tubular necrosis may be obscured by the patient’s primary disease.
You may first note that the patient’s urine output may be oliguric (less than 400 ml/24 hours)—this occurs in 50% of patients; in the remainder, urine output may be less than 100 ml/24 hours for several days.
Inspection may reveal evidence of bleeding abnormalities such as petechiae and ecchymoses. Hematemesis may occur. The skin may be dry and pruritic and, rarely, a uremic frost may be present. Mucous membranes may be dry, and the breath may have a uremic odor.
The patient may exhibit evidence of central nervous system involvement, such as lethargy, somnolence, confusion, disorientation, asterixis, agitation, myoclonic muscle twitching and, possibly, seizures.
Auscultation may reveal tachycardia and, possibly, an irregular rhythm. Rarely, a pericardial friction rub can be heard, indicating pericarditis. Basilar crackles bilaterally may occur if heart failure is present. Palpation and percussion may reveal abdominal pain, if pancreatitis or peritonitis occurs, and peripheral edema, if heart failure is present. Hypertension may also occur from fluid volume overload.
Fever and chills can signal the onset of infection.
