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INTRODUCTION

Acute kidney injury (AKI) is defined by the impairment of kidney filtration and excretory function over days to weeks (generally known or expected to have occurred within 7 days), resulting in the retention of nitrogenous and other waste products normally cleared by the kidneys. AKI is not a single disease but rather a designation for a heterogeneous group of conditions that share common diagnostic features: specifically, an increase in serum creatinine (SCr) concentration often associated with a reduction in urine volume. It is important to recognize that AKI is a clinical diagnosis and not a structural one. A patient may have AKI with or without injury to the kidney parenchyma. AKI can range in severity from asymptomatic and transient changes in laboratory parameters of glomerular filtration rate (GFR), to overwhelming and rapidly fatal derangements in the ability of the kidney to maintain effective circulating volume regulation, excrete nitrogenous wastes and metabolic toxins, and maintain electrolyte and acid-base composition of the plasma.

EPIDEMIOLOGY

AKI complicates 5–7% of acute-care hospital admissions and up to 30% of admissions to the intensive care unit (ICU). AKI severity is staged based on the magnitude of the rise in SCr and severity and duration of oliguria (Table 310-1). The incidence of AKI has grown by more than fourfold in the United States since 1988 and is estimated to have a yearly incidence of 500 per 100,000 population, higher than the yearly incidence of stroke. Large studies have shown that increases in SCr as low as 0.3 mg/dL in hospitalized patients are independently associated with an approximately fourfold increase in hospital mortality, with higher changes in creatine, and longer duration of elevation associated with greater increased risk of morbidity and mortality. Morbidity of AKI in those admitted to the ICU exceeds 50% in many studies. AKI also has longer term implications even if the patient survives the hospitalization. AKI increases the risk for the development or worsening of chronic kidney disease (CKD) and development of dialysis-requiring end-stage kidney disease (ESKD). AKI may also occur in the community. Common causes of community-acquired AKI include volume depletion, heart failure, adverse effects of medications, obstruction of the urinary tract, or malignancy. The most common clinical settings for hospital-acquired AKI are sepsis, major surgical procedures, critical illness involving heart or liver failure, and nephrotoxic medication administration.

TABLE 310-1Staging of Acute Kidney Injury Severity

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