The incidence of acute kidney injury (AKI) in the intensive care unit (ICU) has increased during the past decade due to increased acuity as well as increased recognition. Early epidemiology studies were confounded by erratic definitions of AKI until recent consensus guidelines (RIFLE and AKIN) standardized its definition. This paper discusses the incidence of AKI in the ICU with focuses on specific patient populations. The overall incidence of AKI in ICU patients ranges from 20% to 50% with lower incidence seen in elective surgical patients and higher incidence in sepsis patients. The incidence of contrast-induced AKI is less (11.5%–19% of all admissions) than seen in the ICU population at large. AKI represents a significant risk factor for mortality and can be associated with mortality greater than 50%. 1. Introduction Acute kidney injury (AKI) (also referred to as acute renal failure) reflects a broad spectrum of clinical presentations ranging from mild injury to severe injury that may result in permanent and complete loss of renal function. The range of severity and variety of causes of AKI has resulted in multiple classification systems complicating diagnosis and subsequent management. The lack of consensus has resulted in a broad range of estimated prevalence in the intensive care unit (ICU) ranging from 1% to 70% depending on the criteria used [54, 55]. The underlying mechanisms of AKI include a decrease in the kidney’s ability to excrete nitrogenous waste, manage electrolytes, regulate intravascular volume, and assist with maintenance of the acid-base status. The clinical effects of AKI depend on the clinical situation but almost invariably increase mortality and morbidity [56, 57]. 2. Measurement of Renal Function Definitions of AKI depend on measurement of serum creatinine (Cr) as a surrogate marker for the glomerular filtration rate (GFR). While inulin remains the gold standard for determination of GFR, it is rarely performed due to the need for continuous intravenous infusion and considerable laboratory resources [58]. Calculation of the GFR is performed based on the serum Cr value despite the fact that Cr has a complex metabolism and many factors can alter serum Cr values [59–64]. High protein intake and medications may increase Cr production independently of renal filtration. Furthermore, Cr secretion in the proximal renal tubules [65, 66] may account for as much as 60% of Cr elimination in patients with renal disease [67]. Medications such as cimetidine, quinidine, and trimethoprim inhibit this process [65], whereas hemodialysis can
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