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FOUNDATION OVERVIEW

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Acute kidney injury (AKI) is when there is a sudden and significant decrease in kidney function. An increase in the serum creatinine (SCr) concentration is the result of accumulation due to a decrease in the glomerular filtration rate (GFR). The diagnosis of AKI is based on the change in SCr from baseline as well as changes in urine production. The kidneys are vulnerable to certain types of injury. First, they are dependent upon the heart and vasculature to deliver sufficient blood supply to drive glomerular filtration. Second, they are exposed to numerous endogenous and exogenous substances that are eliminated from the body via the urine.

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A classification system has been developed to predict the severity of AKI utilizing SCr, calculated GFR, and urine output. AKI is classified into one of five strata via the acronym RIFLE: risk, injury, failure, loss, and end-stage renal disease. The first three categories rate the severity of kidney injury, whereas the last two categories refer to the long-term clinical outcomes. RIFLE is a tool for predicting the outcome of an episode of AKI. Although it has not been validated for predicting all outcomes of AKI, it offers a systematic approach to assess an unpredictable disease state.

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PATHOPHYSIOLOGY AND CLASSIFICATION OF AKI

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Acute kidney injury is classified into three categories; prerenal, intrinsic, and postrenal based on the location and type of damage.

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Prerenal Acute Kidney Injury

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Prerenal implies damage or defect occurring before the kidney. A decrease in blood flow/pressure to the kidneys results in a decrease in intraglomerular pressure, a decrease in GFR, and hypoxia/ischemia within the kidneys. Prerenal AKI can occur with total body fluid overload. However, the important factor is the effective intravascular blood volume, not the total body fluid volume. Patients with heart failure, renal artery stenosis, nephrotic range proteinuria, or advanced liver disease may have an increase in total body water with decreased EABV. This is secondary to decreased cardiac output and/or the fluid shift from the intravascular to extravascular compartment. Although such patients appear fluid overloaded (presenting with edema, rales, ascites), the decrease in EABV results in decreased perfusion to the kidney and may result in prerenal AKI.

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Functional prerenal AKI describes a subtype of prerenal AKI. The mechanism is hypoperfusion and intraglomerular hypotension; however, the pathophysiology occurs at the microscopic level of the glomerulus. Intraglomerular pressure is dependent on the pressure of the blood flow entering the Bowman capsule (via the afferent arteriole) and the pressure of the blood flow leaving the Bowman capsule (via the efferent arteriole) (Figure 38-1). The tone of the afferent arteriole is maintained by vasodilatory prostaglandins such as PGE2 and prostacyclin (PGI2). Agents such as nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit prostaglandin synthesis may cause vasoconstriction of the afferent arteriole and therefore decrease the pressure ...

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