Acute tubular necrosis (ATN) is a common diagnosis in acute renal failure, which is a rapidly progressing azotemia (increase in BUN/creatinine) that is often reversible. In order to effectively diagnose ATN, understanding the causes is helpful. There are many causes, but the following will be most encountered and associated with the practice of anesthesiology. ATN can be caused by ischemia, which can be encountered in hypovolemia or highly reduced mean arterial pressures. ATN might also be caused by direct renal tubular toxicity from contrast dyes, certain drugs, myoglobinuria, and hemoglobinuria (blood transfusion reaction).
Once one has determined that a patient has acute kidney injury, there are various tests to determine if ATN is the cause. One can sometimes visualize epithelial cell casts, muddy brown casts, and even free tubular epithelial cells in urine microscopy (this is not 100% sensitive or specific). One can use the fractional excretion of sodium (FENa) to differentiate between pre-renal AKI and ATN. A FENa above 2% is more indicative of ATN, whereas a FENa of less than 1% is commonly associated with pre-renal disease. The gold standard of differentiating between pre-renal AKI and ATN is response to fluid resuscitation. If a patient is hypovolemic with AKI and fluid resuscitated, the patient’s creatinine should return to its baseline within 24-72 hours if the AKI is pre-renal. The BUN:creatinine ratio can be used to diagnose ATN, although this is less specific. The BUN:Cr ratio is commonly normal (10:1-15:1) with ATN, and it is usually >20:1 in pre-renal AKI. The rise of the patient’s creatinine affected by ATN is commonly more than 0.3-0.5 mg/dL each day (then in reversible disease, the creatinine will peak and trend down). Patients with ATN often lose the ability to concentrate urine, which results in them having normal or larger than expected urine output and a lower urine osmolality (less than 450 mosmol/kg and often less than 350 mosmol/kg).