Acute Tubular Necrosis Clinical Presentation

The patient’s history is very important in the diagnosis of acute tubular necrosis (ATN). It frequently reveals recent hypotension, sepsis, muscle necrosis, or volume depletion, as well as exposure to nephrotoxic agents. Patients with rhabdomyolysis present with severe muscle pains and generalized soreness.

ATN is more likely to occur in patients with a history of recent surgery, sepsis, or hypovolemia. The history is also important in establishing risk factors for the development of ATN.

Physical examination findings may be unremarkable because acute kidney injury (AKI) is often found incidentally on routine laboratory studies (ie, elevated blood urea nitrogen [BUN] and creatinine levels). However, if symptoms are present, they may include a pericardial friction rub, asterixis, and/or excoriation marks related to uremic pruritus. Hypertension or edema may be noted.

Otherwise, the physical examination findings are more likely to reflect the underlying disease process. For example, in a patient with rhabdomyolysis, physical examination may disclose tender “doughy” muscles, with significant edema of the involved extremities. In severe cases, compartmental compression syndromes, particularly characterized by neurovascular compromise, may occur.

The 2011 UKRA AKI guidelines state that physiological observation should be performed for all patients with AKI to find early signs of physiological deterioration that may require a rise in the level of care.^[2]

Complications of ATN include fluid and electrolyte imbalances, uremia, infections, and anemia. Specific imbalances vary with the phase of illness; during oliguria, salt and water retention often leads to hypertension, edema, and heart failure. The polyuric phase of ATN may lead to hypovolemia and create a setting for prerenal azotemia and perpetuation of ATN.

Altered fluid and electrolyte balance

Clearly, the maintenance of fluid and electrolyte balance is critical. Hyperkalemia can be associated with life-threatening cardiac arrhythmias (eg, ventricular tachycardia or fibrillation, complete heart block, bradycardia, asystole). Arrhythmias have been reported in up to 30% of patients. On electrocardiography (ECG), hyperkalemia manifests as peaked T waves, prolonged PR interval, P wave flattening, and a widened QRS complex.

In addition to these worrisome cardiac effects, hyperkalemia can also lead to neuromuscular dysfunction and, potentially, respiratory failure. Hyperkalemia can be treated with glucose and insulin, binding resins, or, if necessary, dialysis.

Hyponatremia causes concern because of its effects on the central nervous system. In general, correction of hyponatremia should be of sufficient rapidity and magnitude as to reverse the manifestations of hypotonicity, but not be so rapid or large as to potentiate the risk of osmotic demyelination. The most recent guidelines^[4] that have been published regarding treatment of hyponatremia recommend the rate of correction (of hyponatremia) to be limited to less than 10-12 mmol/L in 24 hours and/or less than 18 mmol/L in 48 hours. Go to Hyponatremia for complete information on this topic.

Other electrolyte disturbances include hyperphosphatemia, hypocalcemia, and hypermagnesemia. Hypocalcemia may be secondary to both deposition of calcium phosphate and reduced levels of 1,25-dihydroxyvitamin D. It is usually asymptomatic, but hypocalcemia may result in nonspecific ECG changes, muscle cramps, or seizures.

In rhabdomyolysis, hypocalcemia results from deposition of calcium in the injured muscle. Such deposited calcium is eventually released back into the circulation during the recovery phase, thereby accounting for transient hypercalcemia. For this reason, calcium administration is generally not recommended for hypocalcemia during the acute phase of rhabdomyolysis, unless the patient is symptomatic.

The 2011 UKRA guidelines recommend administering 0.9% sodium chloride and sodium bicarbonate for intravenous volume expansion in patients at risk of developing AKI secondary to rhabdomyolysis.^[2] Metabolic acidosis may occur. It may be treated with bicarbonate or dialysis as well.

Uremia

Uremia results from the accumulation of nitrogenous waste. It is a potentially life-threatening complication associated with AKI. This may manifest as pericardial disease, gastrointestinal symptoms (ie, nausea, vomiting, cramping), and/or neurologic symptoms (ie, lethargy, confusion, asterixis, seizures). Platelet dysfunction is common and can lead to life-threatening hemorrhage.

Infections

Aggressive treatment of infections is prudent. Infections remain the leading cause of morbidity and mortality and can occur in 30-70% of patients with AKI. Infections are more likely in these patients because of an impaired immune system (eg, uremia, inappropriate use of antibiotics) and because of increased use of indwelling catheters and intravenous needles.

Anemia

Anemia may develop from many possible causes. Erythropoiesis is reduced in AKI. Patients with ATN-related uremia may have platelet dysfunction and subsequent hemorrhage leading to anemia. In addition, volume overload may lead to hemodilution, and red cell survival time may be decreased. Anemia can be corrected with blood transfusions.