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Acute kidney injury (AKI) is the deterioration of renal function over hours or days, resulting in the accumulation of toxic wastes and the loss of internal homeostasis. Definitions based on renal function are listed in Table 88-11-4; AKI is classified using the Risk, Injury, Failure, Loss, and End-Stage Renal Failure (RIFLE),2 the Acute Kidney Injury Network (AKIN),3 and the Kidney Disease: Improving Global Outcomes (KDIGO)4 classifications. These definitions assume that renal function has reached a steady state, which limits their applicability to ED patients with AKI whose renal function may be deteriorating.

TABLE 88-1AKIN and RIFLE Criteria for Acute Kidney Injury

Reversible mechanisms, such as volume depletion, medications, infection, or urinary obstruction,5-9 cause the majority of community-acquired AKI cases presenting to the ED (55% to 79%).5,6,10-12 Despite favorable renal recovery rates, community-acquired AKI is associated with significant hospital mortality, from 7.3% to 19.6%,13,14 and 3-year mortality is as high as 45% to 66%.7,14,15 Hospital-acquired AKI by definition occurs or worsens in the hospital, where mortality ranges from 27% to 62%.6,10,12 For both types of AKI, mortality has a graded relationship with advancing age and severity of AKI.8,16


The functions of the kidneys are glomerular filtration, tubular reabsorption, and secretion. Normal glomerular filtration rate (GFR) in early adulthood is approximately 120 mL/min/1.73 m2 and typically decreases by 8 mL/min/1.73 m2 every decade thereafter. The driving force for glomerular filtration is glomerular capillary pressure, which depends on renal blood flow and autoregulation. For most causes of AKI, global or regional decrease in renal blood flow is the final common pathway. Recovery from AKI first depends on restoration of renal blood flow.

Renal insult is classified ...

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