Instruct to summarize the article below, incorporating key points, tables, and numbers while using abbreviations for brevity (e.g., ↑, ↓, ->) retaining clinical data, examples, and classifications. Rewrite this information with headings and side headings and  as succinct bulleted points (<9 words each), Encourage the use of abbreviations,comparison tables and symbols, avoiding repetition. Emphasize prioritizing accuracy and relevance, ensuring integrity in clinical data. Deliver the output in a well-designed markdown format,should be consistent with the information provided in the article;-
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Definition of acute renal failure
The term acute renal failure is a non-specific
description of an acute, sustained decrease in
renal function. There is a wide spectrum of
severity of acute renal injury ranging from mild
reversible impairment to severe dysfunction
necessitating renal replacement therapy (RRT).
An international interdisciplinary collaborative
group, the Acute Dialysis Quality Initiative
(ADQI), has recently formulated a standard
grading system for acute renal dysfunction.3 The
term acute renal dysfunction encompasses the
full range of abnormalities of renal function.
The acronym RIFLE defines three grades of
increasing severity of acute renal dysfunction
(R, risk; I, injury; F, failure) and two outcome
variables (L, loss; E, end-stage) that are based
on the change in serum creatinine or urine
output (Table 1). The RIFLE criteria have
undergone evaluation in cardiac surgical patients
and in ICU patients, and have been shown to
appropriately define acute renal dysfunction. The
term acute kidney injury (AKI) has been
recently proposed to define the full spectrum of
severity of acute renal dysfunction.4
Pathophysiology
The aetiology of ARF is classically divided
into pre-renal, renal, and post-renal causes. The
majority of cases of ARF in surgical and critically ill patients are because of intrinsic renal
causes; acute tubular necrosis (ATN), which is
typically caused by ischaemic or toxic processes, is the most common.
Acute tubular necrosis
A combination of microvascular and tubular
injury contribute to the development of ATN.5
Intra-renal vasoconstriction because of local
vasoactive mediators, activation of tubuloglomerular feedback, structural endothelial damage,
and leucocyte activation all lead to microvascular damage. Mechanisms of tubular injury
include epithelial apoptosis and necrosis, tubular
obstruction, and transtubular leak of glomerular
filtrate. Inflammatory responses induced by renal
ischaemia–reperfusion injury also play a significant role in the development of ATN.
Nephrotoxic agents
Nephrotoxic agents commonly used in perioperative patients include non-steroidal antiinflammatory drugs, angiotensin-converting
enzyme inhibitors, aldosterone-receptor
Key points
Perioperative acute renal
failure is a common
complication of major
surgery and is associated
with increased morbidity
and mortality.
Ischaemia- or toxinmediated acute tubular
necrosis is the primary
cause of perioperative acute
renal failure.
The key nonpharmacological strategies
are intravascular volume
expansion, maintenance of
renal blood flow and renal
perfusion pressure,
avoidance of nephrotoxic
agents, careful glycaemic
control, and the appropriate
management of postoperative complications.
At present, there is no firm
evidence to suggest that the
use of any specific
pharmacological
intervention is clinically
beneficial.
Dopamine infusion has not
been shown to prevent
acute renal failure, avert the
need for renal replacement
therapy, or reduce
mortality, and should not be
administered solely for renal
protection.
Stephen T Webb FRCA
Specialist Registrar in Anaesthesia and
Intensive Care
Belfast Health and Social Care Trust,
Royal Hospitals
Grosvenor Road
Belfast
BT12 6BA
UK
J Stephen D Allen FCARCSI MD
Consultant in Cardiothoracic Anaesthesia
& Intensive Care
Belfast Health and Social Care Trust,
Royal Hospitals
Grosvenor Road
Belfast
BT12 6BA
UK
Tel: þ44 28 906 34006
Fax: þ44 28 903 25725
E-mail: <PRESIDIO_ANONYMIZED_EMAIL_ADDRESS>
(for correspondence)
176
doi:10.1093/bjaceaccp/mkn032 Advance Access publication August 22, 2008
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antagonists, i.v. radio-contrast agents, aminoglycoside and betalactam antibiotics, amphotericin B, and cyclosporin.
Cardiac and vascular surgery
Several specific factors are involved in the development of ARF
related to cardiac and vascular surgery:
1. Renal hypo-perfusion outside the limits of auto-regulatory
reserve, particularly during cardiopulmonary bypass (CPB), is a
major determinant of ATN.
2. The systemic inflammatory response syndrome (SIRS) triggered
by major surgery results in cell-mediated and cytotoxic injury.
3. ATN may also be exacerbated by renal embolic injury: aortic
atheroma disrupted by operative manipulation and thrombus,
air, lipid, and tissue may contribute to the embolic load during
surgery.
4. Prolonged surgery produces haemolysis: renal excretion of
haem derivatives may result in renal tubular injury.
5. Toxic injury from the administration of nephrotoxic drugs may
also contribute to post-operative ARF. Patients who present for
non-elective cardiac surgery shortly after pre-operative cardiac
catheterization are at increased risk related to both the radiocontrast load and surgery itself. Endovascular aortic surgery is also
associated with ARF because of the administration of a large
dose of contrast.
Risk factors
Evidence from epidemiological studies has established the major
risk factors for perioperative ARF (Table 2). Two risk stratification
tools for ARF after cardiac surgery have recently been tested
and validated.6, 7 Similar risk scoring systems for ARF after noncardiac surgery are under development. The incidence is increasing
because of the increasing age of the surgical population and the
performance of more complex surgery.
Prevention
The identification of high-risk patients and the implementation of
prophylactic measures are the goals of perioperative renal protection. Strategies to reduce the occurrence of renal injury in patients
without evidence of acute renal dysfunction are referred to as
primary prevention. The avoidance of additional renal injury in the
setting of established acute renal dysfunction is termed secondary
prevention. Both non-pharmacological and pharmacological interventions may be considered.
Non-pharmacological strategies
These include intravascular volume expansion, maintenance of
renal blood flow and renal perfusion pressure, avoidance of nephrotoxic agents, strict glycaemic control, and appropriate management
of post-operative complications.
Intravascular volume expansion
Perioperative hypovolaemia should be rapidly corrected by volume
expansion with i.v. fluids, whether occurring before, during, or
after surgery. The role of crystalloids compared with colloids for
intravascular volume expansion remains unclear. Although not a
primary outcome measure, a large multi-centre trial of fluid resuscitation in critically ill patients found no difference between
albumin and 0.9% sodium chloride in terms of the risk of ARF.
The renal effects of different colloids have not yet been fully
elucidated. Albumin and gelatin appear to be safe in patients with
normal renal function. The safety of hydroxyethyl starch solutions
in the setting of established renal impairment has not been clarified. Recent evidence suggests that hydroxyethyl starch is associated with a higher incidence of ARF than Ringer’s lactate in
critically ill patients with severe sepsis.
Table 2 Risk factors for perioperative acute renal failure. IABP, intra-aortic balloon
pump; CPB, cardiopulmonary bypass
Pre-operative factors Intra-operative factors Post-operative factors
Chronic disease Type of surgery Acute conditions
Advanced age Cardiac Acute cardiac
dysfunction
Female sex Aortic Haemorrhage
Chronic renal disease Peripheral vascular Hypovolaemia
Diabetes mellitus Non-renal solid organ
transplantation
Sepsis
Chronic cardiac failure Cardiac surgery Rhabdomyolysis
Aortic and peripheral
vascular disease
Prolonged CPB time Intra-abdominal
hypertension
Chronic liver disease Combined procedures Multiple organ
dysfunction syndrome
Genetic pre-disposition Emergency surgery Drug nephrotoxicity
Acute conditions
Hypovolaemia Previous cardiac surgery
Sepsis Aortic surgery
Preoperative IABP Aortic clamp placement
Multiple organ
dysfunction syndrome
Intra-operative
radiocontrast
Drug nephrotoxicity
Table 1 The RIFLE classification of acute renal dysfunction. GFR, glomerular
filtration rate; UO, urine output; ARF, acute renal failure; ESRD, end-stage renal
disease
Grade Glomerular filtration rate
criteria
Urine output criteria
R, Risk Serum creatinine increase:
1.5-fold; GFR decrease:
.25%
UO ,0.5 ml kg21 h21 for 6 h
I, Injury Serum creatinine increase:
2-fold; GFR decrease: .50%
UO ,0.5 ml kg21 h21 for 12 h
F, Failure Serum creatinine increase:
3-fold; GFR decrease:
.75%; serum creatinine
decrease: .350 mmol litre21
(4 mg dl21
) with acute
increase .44 mmol litre21
(0.5 mg dl21
)
UO ,0.3 ml kg21 h21 for 24 h
or anuria for 12 h
L, Loss Persistent ARF¼complete loss of renal function for .4 weeks
E, End-stage ESRD¼complete loss of renal function for .3 months
Perioperative renal protection
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The benefit of isotonic i.v. fluid expansion for the prevention of
radiocontrast-induced nephropathy has been clearly demonstrated.
However, the ideal composition of such fluid and the optimal rate
of infusion have not been determined and should be individualized.
Surgical patients receiving contrast will benefit from the use of the
lowest possible volume of non-ionic, iso-osmolar contrast in conjunction with isotonic i.v. fluids.
Maintenance of renal blood flow and renal
perfusion pressure
Maintenance of adequate renal blood flow and perfusion pressure
involves the defence of both cardiac output and systemic arterial
pressure. The initial approach should be intravascular volume
expansion to reverse hypovolaemia. Inotropic and vasopressor
therapy may then be initiated for the management of low cardiac
output and systemic arterial hypotension, respectively. Despite
historic concerns, norepinephrine is an excellent first-line vasopressor agent. There is no firm evidence to suggest that the drug
compromises renal, hepatic, or gastrointestinal blood flow when
used to treat arterial hypotension. Vasopressin and terlipressin
may be useful agents in the treatment of post-operative
catecholamine-resistant vasodilatory shock. The optimal therapeutic target for systemic arterial pressure for renal protection has
not been established. A minimum mean arterial pressure of 65–75
mm Hg is often targeted in clinical practice; however, a higher
target may be necessary in patients with pre-existing hypertension.
Avoidance of nephrotoxic drugs
Minimizing perioperative exposure to nephrotoxic drugs is crucial
in the prevention of ARF. The use of once-daily aminoglycoside
dosing and the use of lipid formulations of amphotericin B have
been demonstrated to lower the risk of nephrotoxicity associated
with these drugs. There are concerns regarding the risk of renal
injury associated with the antifibrinolytic agent aprotinin. Recent
controversial evidence suggests that the use of aprotinin during
coronary artery bypass graft (CABG) surgery may be associated
with an increased risk of ARF requiring dialysis.
Glycaemic control
Strict glycaemic control using intensive insulin therapy improved
survival and reduced the incidence of ARF requiring RRT in a
landmark trial in mechanically ventilated surgical ICU patients.
Perioperative hyperglycaemia during cardiac and vascular surgery
is associated with increased renal morbidity and overall mortality.
Although the current evidence suggests that strict normoglycaemia
is required for optimum benefit, this approach increases the risk of
hypoglycaemia, the clinical significance of which is unknown in
the ICU setting. It is not yet clear whether rigorous intra-operative
glycaemic control reduces morbidity and mortality in patients
undergoing cardiac and vascular surgery