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ESSENTIALS OF DIAGNOSIS
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GENERAL CONSIDERATIONS
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AKI is defined as an absolute increase in serum creatinine by 0.3 mg/dL or more over 48 hours, or a relative increase of 1.5 times baseline or more that is known or presumed to have occurred within 7 days. It is characterized as oliguric if urine production is less than roughly 400–500 mL/day. 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/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 kidney replacement therapy. In the absence of functioning kidneys, serum creatinine will typically increase by 1–1.5 mg/dL daily, although in 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. Patients with AKI from any cause are at higher risk for all-cause mortality even if there is substantial renal recovery.
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A. Symptoms and Signs
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Although most patients will not experience any symptoms or exhibit any signs of AKI, profound 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. Uremia rarely causes a hemorrhagic pericarditis resulting in a friction rub on auscultation and possible tamponade if the effusion is large. Hyperkalemia may occur, with its attendant risk of heart block and ventricular tachycardia. Prolonged bleeding time due to platelet dysfunction may be seen with uremia. Progressive uremia may also cause neurologic signs such as asterixis, encephalopathy, and seizures.
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B. Laboratory Findings
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By definition, elevated serum creatinine levels are present. Metabolic acidosis (due to decreased clearance of ...