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Prerenal azotemia and acute tubular necrosis account for the overwhelming majority of hospital-acquired acute kidney injury cases, whereas acute glomerulonephritis and vasculitides are relatively more common causes of acute kidney injury developing outside the hospital.
Acute kidney injury occurs in at least 10% to 30% of patients admitted to an ICU, and severe AKI is associated with a mortality rate of about 50%, despite advances in supportive care and technology.
Traditionally, the most important diagnostic classification to be made in the evaluation of patients with acute kidney injury is based on the site of the renal lesion (pre-, intra-, or postrenal).
Since there are few specific therapies available in patients with established acute tubular necrosis, the major clinical focus is on prevention of AKI by identification of subjects at highest risk.
All aspects of treatment of acute tubular necrosis, including renal replacement therapy, are basically supportive. The nondialytic measures of greatest importance are maintenance of nutritional, volume, and electrolyte homeostasis.
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Acute renal failure (ARF) is defined as a rapid decline (over hours to days) in glomerular filtration rate (GFR). This manifests as a rapid increase in blood urea nitrogen (BUN; “azotemia”) and serum creatinine, and may or may not be accompanied by a decline in urine output.1 The concept of acute renal failure has undergone significant change over the last number of years. Lack of standardization in the definition of acute renal failure and the emergence of evidence that even small increases in serum creatinine are associated with increased mortality has led to widespread adoption of diagnostic criteria for the term acute kidney injury (AKI).2 AKI has largely replaced the term acute renal failure (ARF). It is a syndrome that includes minor degrees of injury as well as more severe renal failure, and does not allude to the mechanism of injury. Glomerular filtration rate (GFR) is the best measure of kidney function, but is not easily measured in clinical practice. A change in serum creatinine or urine output is used as a marker for a change in GFR and forms the basis for the various diagnostic criteria for AKI.
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A number of classification systems for AKI exist; the most widely validated is the RIFLE system.3,4 This classification system was proposed by the Acute Dialysis Quality Initiative (ADQI) in 2004.5 The acronym RIFLE represents three severity of injury classes: risk, injury, and failure, and two outcomes: loss of function and end-stage renal disease (Fig. 97-1). The severity of injury is defined by the magnitude of increase in serum creatinine from a baseline value (within a 7-day period or less), or a reduction in urine output for a defined period of time. The outcomes are defined by the duration of kidney injury. Criticisms of the RIFLE classification include the need for a baseline creatinine value to define a case of AKI, and a lack of clarity concerning the ...