We searched PubMed and Medline between Jan 6, 2011, and Sept 13, 2011, for articles in English with the terms “acute kidney injury”, “acute renal failure”, “continuous hemofiltration”, “continuous renal replacement therapy”, and “haemodialysis”. We combined the terms “continuous hemofiltration”, “continuous renal replacement therapy”, and “haemodialysis” with “acute kidney injury” and “acute renal failure”. We did not restrict articles by date of publication. We identified 5523 potentially
SeminarAcute kidney injury
Introduction
Acute kidney injury is the new consensus term for acute renal failure.1 It refers to a clinical syndrome characterised by a rapid (hours to days) decrease in renal excretory function, with the accumulation of products of nitrogen metabolism such as creatinine and urea and other clinically unmeasured waste products. Other common clinical and laboratory manifestations include decreased urine output (not always present), accumulation of metabolic acids, and increased potassium and phosphate concentrations.
The term acute kidney injury has replaced acute renal failure to emphasise that a continuum of kidney injury exists that begins long before sufficient loss of excretory kidney function can be measured with standard laboratory tests. The term also suggests a continuum of prognosis, with increasing mortality associated with even small rises in serum creatinine, and additional increases in mortality as creatinine concentration rises.
Section snippets
Epidemiology
The described notions have led to a consensus definition of acute kidney injury by the Acute Dialysis Quality Initiative. These RIFLE (risk, injury, failure, loss, end stage) criteria (figure 1)1 have been broadly supported with minor modifications by the Acute Kidney Injury Network,2 and both definitions have now been validated in thousands of patients3 and seem to work similarly to each other. A new consensus definition merging the RIFLE criteria and the Acute Kidney Injury Network definition
Key ideas
Most clinicians are familiar with two key ideas related to acute kidney injury—namely, acute tubular necrosis and prerenal azotaemia. Acute tubular necrosis describes a form of intrinsic acute kidney injury that results from severe and persistent hypoperfusion of the kidneys (ie, prerenal acute kidney injury), although the term secondary acute kidney injury might be more appropriate. This definition is widely accepted and used in textbooks and by clinicians. However, we have some serious
Pathophysiology
The pathogenesis of inflammatory diseases of the kidney parenchyma (eg, glomerulonephritis and vasculitis) is complex and implicates almost all aspects of the innate inflammatory system and antibody-mediated and immune-cell-mediated mechanisms.11, 12, 13, 14, 15, 16, 17 In this Seminar, we focus on acute kidney injury secondary to prerenal factors because this form is the most common in developed countries, in hospital inpatients, and particularly in critically ill patients.
Much of our
Neurohormonal mechanisms
Sympathetic system activation41 and neurohormonal responses unique to the kidney are activated in acute kidney injury.42 The renin–angiotensin–aldosterone system,43 renal sympathetic system,42 and tubuloglomerular feedback system43 are activated. Knowledge of these changes has led to schemata of how acute kidney injury can be precipitated in human beings (figure 2). These frameworks show that, in situations such as sepsis, infection leads to induction of nitric oxide synthase and
Diagnosis
Because acute kidney injury is asymptomatic until extremes of loss of function are reached and has no characteristic clinical findings, diagnosis typically occurs in the context of another acute illness. Although oliguria is a helpful sign, it is neither specific nor sensitive.48 Under most circumstances, acute kidney injury is diagnosed in high-risk contexts (eg, sepsis, major surgery, bleeding, volume losses) by laboratory tests. Creatinine and urea concentrations are the standard diagnostic
Nephrotoxic drugs
Drug-induced acute kidney injury is important because the offending drug can often be identified and removed or substituted for one that is non-nephrotoxic or less nephrotoxic. Additionally, many affected patients present with polyuric acute kidney injury, and thus a high index of suspicion is crucial for diagnosis. Drugs seem to contribute to acute kidney injury in roughly 20% of patients, especially in critically ill patients.59, 60 Panel 1 shows a list of frequently prescribed drugs that are
Laboratory assessment of renal function
The laboratory hallmarks of acute kidney injury are increased serum creatinine concentrations or raised plasma urea concentrations, or both. Unfortunately, these waste products are insensitive markers of glomerular filtration rate and are modified by nutrition, use of steroids, presence of gastrointestinal blood, muscle mass, age, sex, muscle injury, and aggressive fluid resuscitation. Furthermore, they become abnormal only when glomerular filtration rate decreases by more than 50% and do not
Novel biomarkers
Investigators have used new search techniques based on proteomics to identify several novel biomarkers of acute kidney injury. Despite the novelty and dynamic nature of this new research specialty,67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89 several key points can already be made. First, in patients who develop acute kidney injury, concentrations of these biomarkers seem to change earlier than do serum creatinine concentrations (figure 3).82
Prevention
The fundamental principle of prevention of acute kidney injury is to treat the cause or trigger. If prerenal factors contribute, they should be identified, haemodynamic resuscitation quickly begun, and intravascular volume maintained or rapidly restored. In many patients, insertion of a peripheral intravenous catheter and rapid administration of intravenous fluids are sufficient to complete this process. The choice of fluid for such resuscitation is controversial. In particular, the possibility
General management
The principles of management of established acute kidney injury are to treat or remove the cause and to maintain homoeostasis while recovery takes place. Complications can be prevented in some cases by actions that vary in complexity from fluid restriction to extracorporeal renal replacement therapy. Most experts recommend that nutritional support should be started early, contain adequate calories and protein, and be given as for other hospital inpatients or those in intensive-care units. No
Prognosis
Mortality from acute kidney injury remains high, particularly in critically ill patients, in whom mortality was 53% in the ATN trial and 44·7% in the RENAL trial. Several large epidemiological studies have linked acute kidney injury with the later development of chronic kidney disease, end-stage kidney disease, and mortality.135, 136, 137, 138, 139, 140, 141 These results suggest that even a short episode of acute illness might contribute to long-term morbidity and mortality. Thus, the cost to
Search strategy and selection criteria
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