The first description of ARF, then termed ischuria renalis, was by William Heberden in 1802.25 At the beginning of the twentieth century, ARF, then named Acute Bright’s disease, was well described in William Osler’s Textbook for Medicine (1909), as a consequence of toxic agents, pregnancy, burns, trauma, or operations on the kidneys. During the First World War the syndrome was named”war nephritis”26, and was reported in several publications. The syndrome was forgotten until the Second World War, when Bywaters and Beall published their classical paper on crush syndrome.27 However, it is Homer W. Smith who is credited for the introduction of the term ”acute renal failure”, in a chapter on ”Acute renal failure related to traumatic injuries” in his textbook The kidney-structure and function in health and disease (1951). Unfortunately, a precise biochemical definition of ARF was never proposed and, until recently, there was no consensus on the diagnostic criteria or clinical definition of ARF, resulting in multiple different definitions.
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DEFINITION AND CLASSIFICATION
Acute kidney injury (AKI) is a protean syndrome of varied severity. It is characterized by a rapid (hours to weeks) decline in the glomerular filtration rate (GFR) and retention of nitrogenous waste products such as blood urea nitrogen (BUN) and creatinine.2,3 In recent years, it has been recognized that the time-honored term acute renal failure (ARF) fails to adequately describe what is a dynamic process extending across initiation, maintenance, and recovery phases, each of which may be of variable duration and severity. The term acute renal failure suggests that the syndrome is dichotomous and places an undue emphasis on whether or not renal function has overtly failed. This belies the now well-established fact that even mild decrements in glomerular filtration may be associated with adverse clinical outcomes.28-32 The alternative proposed term acute kidney injury has much to recommend it, perhaps better captures the diverse nature of this syndrome, and has entered into widespread clinical use.
Historically, patients with AKI have been classified as being nonoliguric (urine output >400 mL/day), oliguric (urinary out-put <400 mL/day), or anuric (urinary output <100 mL/day).33 Lower levels of urinary output typically reflect a more severe initial injury, have implications for volume overload and electrolyte disturbances, and are of prognostic importance. However, the therapeutic manipulation of the urine output does not ameliorate this prognostic association.
For purposes of diagnosis and management, AKI has been divided into three categories34
1. Diseases characterized by renal hypoperfusion in which the integrity of renal parenchymal tissue is preserved (prerenal states),
2. Diseases involving renal parenchymal tissue (intrarenal AKI or intrinsic AKI), and
3. Diseases associated with acute obstruction of the urinary tract (postrenal or obstructive AKI).
Most acute intrinsic AKI is caused by ischemia or nephrotoxins and is classically associated with ATN.
AKI may occur in someone either with previously normal renal function or as an acute and unanticipated deterioration in function in the setting of previously established chronic kidney disease.
The etiology and outcome of AKI is heavily influenced by the circumstances in which it occurs, such as whether it develops in the community or in the hospital. It is similarly important to distinguish whether the kidney injury occurs as an isolated process, which is more common in community-acquired AKI, or if it occurs as part as a more extensive multiorgan syndrome. In the former context, management is often, at least initially, conservative and follows an expectant approach-deferring renal replacement therapy when possible while awaiting the spontaneous recovery of renal function. In the case of a critically ill patient with multiorgan failure, dialysis may be commenced much earlier, because the goal is not simply control of azotemia but rather one of renal support in an attempt to optimize the subject’s physiologic parameters.35
More than 35 different definitions of AKI have been used in the recent literature.36 In 2004, the Acute Dialysis Quality Initiative (ADQI)1,19-23 group, comprising experts in the fields of nephrology and critical care medicine, published the RIFLE classification, a new consensus and evidence-based definition for AKI.1 The RIFLE classification defines three grades of severity of AKI (Risk, Injury and Failure) based on changes to serum creatinine and urine output and two clinical outcomes (Loss, End-stage).
The classification system includes separate criteria for creatinine and urine output (UO). A patient can fulfill the criteria through changes in serum creatinine (SCreat) or changes in UO, or both. The criteria that lead to the worst possible classification should be used.
The acronym RIFLE stands for the increasing severity classes Risk, Injury, and Failure; and the two outcome classes, Loss and End-Stage Renal Disease (ESRD). The three severity grades are defined on the basis of the changes in SCr or urine output where the worst of each criterion is used. The two outcome criteria, Loss and ESRD, are defined by the duration of loss of kidney function.As of early 2010, over half a million patients have been studied to evaluate the RIFLE criteria as a means of classifying patients with AKI.37-39
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In 2007, the Acute Kidney Injury Network (AKIN), an international network of AKI researchers, organized a summit of nephrology and critical care societies from around the world. The group endorsed the RIFLE criteria with a small modification to include small changes in SCr (> 0.3 mg/dl or > 26.5 mmol/l) when they occur within a 48-hour period.24 Two recent studies examining large databases in the USA40 and Europe41 validated these modified criteria. Thakar et al. found that increased severity of AKI was associated with an increased risk of death independent of comorbidity.40
Diagnostic criteria for acute kidney injury24
An abrupt (within 48 hours) reduction in kidney function currently defined as an absolute increase in serum creatinine of more than or equal to 0.3 mg/dl (≥ 26.4 μmol/l), a percentage increase in serum creatinine of more than or equal to 50% (1.5-fold from baseline), or a reduction in urine output (documented oliguria of less than 0.5 ml/kg per hour for more than six hours).
A major challenge in the investigation and management of AKI is the timely recognition of the syndrome. It remains difficult to easily and reliably measure rapid changes in the GFR. Although the severity in decline in GFR correlates with the onset of oliguria, the latter is insensitive marker of the syndrome because many subjects with severe renal failure remain nonoliguric. In AKI, there is poor agreement between serum creatinine and GFR, at least until a serum creatinine steady state is reached, and even then, the absolute rise in serum creatinine must take into account differences in creatinine generation rates.42 As a result, definitions of AKI that are based on a fixed increment in serum creatinine would be expected to be biased toward making an early diagnosis in well-muscled as compared with malnourished subjects or in men as compared with women. Creatinine clearances, especially when measured over a short time frame such as 2 to 4 hours, has some utility but may substantially overestimate GFR at low levels of renal function owing to a relatively high proportion of tubular secretion. Even the use of markers such as iothalamate to estimate GFR may be less precise in the acute as compared with the chronic setting owing to alterations in their volume of distribution as well as issues relating to tubular obstruction and backleak.
Acute kidney injury is a common and important diagnostic and therapeutic challenge for clinicians.43The incidence of AKI is difficult to estimate because no registry of its occurrence exists and because up until recently there was no standardized definition. From a variety of predominantly single center studies it is estimated that 5% to 7% of hospitalized patients develop AKI.44-47 More detailed information is available regarding its development in the intensive care unit (ICU) environment, where approximately 25% to 30% of unselected patients develop some degree of AKI, although again estimates vary considerable depending on the definition used and the population casemix. Renal replacement therapy is typically required in 5% to 6% of the general ICU population or 8.8 to 13.4 cases per 100,000 population/year.30,43,48-53 AKI is also a major medical complication in the developing world, particularly in the setting of diarrheal illnesses, infectious diseases like malaria and leptospirosis, and natural disasters such as earthquakes. 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%.44
AKI IN THE DEVELOPING WORLD
The epidemiology of AKI differs tremendously between developed and developing countries, owing to differences in demographics, economics, geography, and comorbid disease burden. While certain features of AKI are common to both-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.44Factors responsible for this higher incidence of AKI in the tropics include hot climate in conjunction with excessive sweating, increased predisposition to hypovolemic insults, poor nutritional status and increased susceptibility to infections.
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