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FOUNDATION OVERVIEW

Acute kidney injury (AKI) occurs 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 and/or changes in urinary output (UOP). AKI can occur because 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, which are eliminated from the body via the urine.

A classification system has been developed to describe the severity of AKI utilizing SCr, estimated GFR, and UOP. 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, while the last two categories refer to the time sensitive clinical outcomes. Both AKI defined by the RIFLE criteria and increasing severity of AKI have been associated with increased mortality rates.

PATHOPHYSIOLOGY AND CLASSIFICATION OF ACUTE KIDNEY INJURY

AKI is classified into three types based on location and type of injury: prerenal, intrinsic, and postrenal. Many medications can cause or worsen various types of AKI (Table 34-1).

TABLE 34-1Medications Associated With Acute Kidney Injury

Prerenal Acute Kidney Injury

Prerenal implies damage or defect occurring before the kidney and is the most commonly encountered type of AKI. A decrease in blood flow/pressure to the kidneys results in a decrease in intraglomerular pressure as well as a decrease in UOP and GFR. Prerenal AKI can occur with total body fluid overload. However, the important factor is the effective arterial blood volume (EABV), 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, ...

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