Abstract

Acute kidney injury (AKI) is defined as a syndrome in which there is an abrupt (hours to days) absolute increase in serum creatinine (SCr) of 0.5 mg/dL or a 25% increase from baseline. Even a modest rise in SCr of 0.3 mg/dL during hospitalization is associated with increased mortality and morbidity. Because of difficulties using SCr as a determinant of AKI, a variety of serum (neutrophil gelatinase–associated lipocalin, interleukin-18) and urine (kidney injury molecule–1) biomarkers of AKI are currently undergoing intense investigation. AKI may be defined pathophysiologically, as a decrease in renal blood flow (prerenal), or an intrinsic renal parenchymal disease (renal), or obstruction of urine flow (postrenal). Indications for emergent dialysis include hyperkalemia, fluid overload, acidosis, and signs and symptoms of uremia. If AKI is diagnosed in the emergency department, the patient should be admitted for further workup. In the majority of patients who survive AKI, renal function essentially returns to normal. Key words: acute kidney injury, dialysis, hyperkalemia, serum creatinine This review contains 3 highly rendered figures, 11 tables, and 49 references.

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