AKI is defined as an absolute increase in serum creatinine by 0.3 mg/dL or more within 48 hours or a relative increase of at least 1.5 times baseline that is known or presumed to have occurred within 7 days. AKI is characterized as oliguric if urine production is less than roughly 400–500 mL/day. Clinically, AKI is characterized by an inability to maintain acid-base, fluid, and electrolyte balance and to excrete nitrogenous wastes. The three stages of AKI defined by the 2012 Kidney Disease Improving Global Outcomes Clinical Practice Guidelines for Acute Kidney Injury are based on the elevation in serum creatinine or decline in urinary output, both of which inform prognosis. Stage 1 is a 1.5- to 1.9-fold increase in serum creatinine or a decline in urinary output to less than 0.5 mL/kg/h over 6–12 hours; stage 2 is a 2.0- to 2.9-fold increase in serum creatinine or decline in urinary output to less than 0.5 mL/kg/h over 12 hours or longer; stage 3 is a 3.0-fold or greater increase in serum creatinine, an increase in serum creatinine to greater than or equal to 4 mg/dL, a decline in urinary output to less than 0.3 mL/kg/h for 24 hours or longer, anuria for 12 hours or longer, or initiation of renal replacement therapy. In the absence of functioning kidneys, serum creatinine concentration will typically increase by 1–1.5 mg/dL daily, although with certain conditions, such as rhabdomyolysis, serum creatinine can increase more rapidly. On average, 5% of hospital admissions and 30% of intensive care unit (ICU) admissions include a diagnosis of AKI, and AKI will develop in 25% of hospitalized patients. Patients with AKI of any type are at higher risk for all-cause mortality according to prospective cohort studies, even if renal recovery is substantial. The rates of AKI in the hospital setting have increased steadily since the 1980s and continue to rise.
A. Symptoms and Signs
Although many patients will not experience any symptoms or exhibit any signs of AKI, the buildup of waste products can sometimes cause nonspecific symptoms and signs collectively termed uremia. Uremia can cause nausea, vomiting, malaise, and altered sensorium. Additionally, patients may experience symptoms and signs of the underlying disease process causing their AKI (eg, lupus). Hypertension can occur, and fluid homeostasis is often impaired. Hypovolemia can cause states of low blood flow to the kidneys, sometimes termed prerenal azotemia, whereas hypervolemia can result from intrinsic or postrenal disease. Pericardial effusions can occur with uremia and may result in cardiac tamponade; a pericardial friction rub can be present, signaling pericarditis. With hyperkalemia, ventricular tachycardia and other tachyarrhythmias can occur. The lung examination may reveal rales in the presence of hypervolemia. AKI can cause nonspecific diffuse abdominal pain and ileus as well as platelet dysfunction; bleeding and clotting disorders are more common in affected ...