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Acute kidney injury (AKI) is defined by the impairment of kidney filtration and excretory function over days to weeks, 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 effective circulating volume regulation and electrolyte and acid-base composition of the plasma.


AKI complicates 5–7% of acute care hospital admissions and up to 30% of admissions to the intensive care unit. 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. AKI is associated with a markedly increased risk of death in hospitalized individuals, particularly in those admitted to the ICU where in-hospital mortality rates may exceed 50%. AKI increases the risk for the development or worsening of chronic kidney disease (CKD). Patients who survive and recover from an episode of severe AKI requiring dialysis are at increased risk for the later development of dialysis-requiring end-stage kidney disease. AKI may be community-acquired or hospital-acquired. 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.


image AKI is also a major medical complication in the developing world, where the epidemiology differs from that in developed countries due to differences in demographics, economics, environmental factors, and comorbid disease burden. While certain features of AKI are common in the developed and developing countries—particularly since urban centers of some developing countries increasingly resemble those in the developed world—many etiologies for AKI are region-specific such as envenomations from snakes, spiders, caterpillars, and bees; infectious causes such as malaria and leptospirosis; and crush injuries and resultant rhabdomyolysis from earthquakes.


The causes of AKI have traditionally been divided into three broad categories: prerenal azotemia, intrinsic renal parenchymal disease, and postrenal obstruction (Fig. 304-1).

FIGURE 304-1

Classification of the major causes of acute kidney injury. ACE-I, angiotensin-converting enzyme inhibitor-I; ARB, angiotensin receptor blocker; NSAIDs, nonsteroidal anti-inflammatory drugs; PPI, proton pump inhibitors; TTP-HUS, thrombotic thrombocytopenic purpura–hemolytic-uremic syndrome.


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