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  • Rapid increase in serum creatinine.

  • Oliguria may be present.

  • Symptoms and signs depend on cause and severity.


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 1.5 times baseline or more 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. 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 degree of 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/hour 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/hour 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/hour for 24 hours or longer, anuria for 12 hours or longer, or initiation of kidney replacement therapy. In the absence of functioning kidneys, serum creatinine will typically increase by 1–1.5 mg/dL daily, although with certain conditions such as rhabdomyolysis serum creatinine can increase more rapidly. Using the AKI stage definition above, AKI is estimated to occur in approximately 20% of all hospitalized patients and 65% of patients in the ICU. Observed rates of AKI in the hospital setting are increasing over time. Patients with AKI from any cause are at higher risk for all-cause mortality according to prospective cohort studies, even if renal recovery is substantial.


A. Symptoms and Signs

Although most patients will not experience any symptoms or exhibit any signs of AKI, accumulation of waste products can cause nonspecific symptoms and signs collectively termed uremia: nausea, vomiting, malaise, and altered sensorium. More commonly, patients experience symptoms and signs of the underlying disease causing their AKI (eg, lupus). Elevated blood pressure 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 develop 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. Platelet dysfunction ...

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