|
|
|
 |
|
 |
 |
| Peter McCullough completed his
medical degree at the University
of Texas Southwestern Medical
School in Dallas, was Resident at
the University of Washington in
Seattle, and gained a cardiology
fellowship at William Beaumont
Hospital in Royal Oak. He earned
a masters degree in public health
at the University of Michigan
in Ann Arbor. At Beaumont
Hospital, Dr. McCullough leads
an active research team that
focuses on disease prevention
and determinants of cardiorenal
disease, including obesity,
cardiac and renal risk factors,
and novel biomarkers. He has
published over 500 medical
communications, including over
300 peer-reviewed manuscripts
and abstracts. Dr. McCullough is
on the editorial boards of Reviews
in Cardiovascular Medicine and
The American Journal of Kidney
Disease. He is an internationally
recognized authority on the role
of chronic kidney disease as a
cardiovascular risk state. |
CIN Consensus Working Panel: Executive Summary
Peter A McCullough, MD, MPH
Consultant Cardiologist, William Beaumont Hospital,
Michigan, USA
Address for correspondence:
Dr Peter A McCullough, MD, MPH
Consultant Cardiologist
William Beaumont Hospital, Coolidge Highway
Royal Oak, Michigan 48073, USA
Tel: +1-248-655-5929 Fax: +1-248-380-2008
Email: pmccullough@beaumont.edu
Abstract
Radiological and cardiological procedures continue to
rely on the use of iodinated contrast media for the
identification of vascular structures. Contrast-induced
nephropathy (CIN) is an important complication in
the use of iodinated contrast media which accounts
for a significant number of cases of hospital-acquired
renal failure, with adverse effects on prognosis and
healthcare costs. CIN is likely to remain a significant
challenge for clinicians since more patients are likely to
undergo exposure to contrast media in the future and
since the incidence of chronic kidney disease, the major
risk factor for CIN, is increasing. The CIN Consensus
Working Panel is an international multidisciplinary
group convened to address the challenges of CIN.
A total of 4370 references were identified by literature
search (the MEDLINE and EMBASE databases from
1966 to February 2005), of which 865 were considered
potentially relevant. The results of the literature
search were used to compile reviews covering the
epidemiology and pathogenesis of CIN, baseline renal
function measurement, risk assessment, identification
of high-risk patients, contrast medium use and
preventive strategies. In this summary of the work of
the panel, the consensus statements and an algorithm
for the risk stratification and management of contrastinduced
nephropathy are presented.
Introduction
Contrast-induced nephropathy (CIN) is an important
complication in the use of iodinated contrast media
which accounts for a significant number of cases of
hospital-acquired acute kidney injury.1-3 This iatrogenic
condition has an adverse effect on prognosis and adds
to healthcare costs. Several factors contribute to the
increasing importance of this subject to radiologists,
cardiologists and nephrologists. The numbers of imaging
and interventional procedures continue to increase
which inevitably means more patients will be exposed
to intravascular iodinated contrast media. At the same
time, the incidence and prevalence of chronic kidney
disease (CKD), the most important risk factor for CIN,
are increasing worldwide.4
The CIN Consensus Working Panel is an international
multidisciplinary group convened to address the
challenges of CIN. The group systematically reviewed
the published evidence on CIN and used this, together
with expert opinion drawn from clinical practice,
to compile a series of consensus statements and a
management algorithm.
CIN Consensus Working Panel
The Working Panel comprised two radiologists, a CT
expert, two cardiologists and two nephrologists practising
in Europe and the USA. At the first meeting in November
2004, the overall scope and strategy for the project
were agreed and at the second in September 2005, the
Working Panel reviewed and discussed all the evidence
and developed a series of consensus statements.
Methodology
A systematic search of the literature was undertaken to
identify all references relevant to the subject of CIN, as
a result of which 865 potentially relevant papers were
identified and reviewed. The results of the literature
search were used to compile reviews covering the
epidemiology and pathogenesis of CIN, baseline renal
function measurement, risk assessment, identification of
high-risk patients, contrast medium use and preventive
strategies.5-11 After reviewing all the evidence, the
Working Panel agreed a series of consensus statements
addressing the identification of patients at risk of CIN
and strategies for reducing the risk (Table 1).12 The results
were also integrated into a proposed algorithm for the
management of patients at risk of CIN (Figure 1).12
Epidemiology and prognostic implications of CIN
Incidence
The reported incidence of CIN varies widely across the
literature, depending on the patient population and the
baseline risk factors. Moreover, as with any clinical event,
the incidence also varies depending on the criteria by
which it is defined. CIN is typically defined in the recent
literature as an increase in serum creatinine occurring
within the first 24 hours after contrast exposure and
peaking up to 5 days afterwards. In most instances,
the rise in serum creatinine is expressed either in
absolute terms (0.51.0 mg/dl; 44.288.4 µmol/l) or as
a proportional rise in serum creatinine of 25% or 50%
above the baseline value. The most commonly used
definition in clinical trials is a rise in serum creatinine
of 0.5 mg/dl (44.2 µmol/l), or a 25% increase from the
baseline value, assessed at 48 hours after the procedure.
The European Society of Urogenital Radiology (ESUR)
defines CIN as impairment in renal function (an
increase in serum creatinine by more than 25%
or 44.2 µmol/l [0.5 mg/dl]) within 3 days after
intravascular administration of contrast medium,
without an alternative aetiology.13 Although other
definitions have been used such as a rise in serum
creatinine >0.3 mg/dl with oliguria, decreases in
glomerular filtration rate (GFR) or creatinine clearance or increases in serum urea nitrogen (BUN), defined
serum creatinine alone changes appear to be the
universal benchmark measure for the occurrence of CIN.
Consensus Statement 1
Contrast-induced nephropathy (CIN) is a common and potentially serious complication following the administration of contrast media in patients
at risk for acute renal injury. |
Consensus Statement 2
The risk of CIN is elevated and of clinical importance in patients with chronic kidney disease (particularly when diabetes is also present), recognised
by an estimated glomerular filtration rate <60 ml/min/1.73 m2. |
Consensus Statement 3
When serum creatinine or estimated glomerular filtration rate is unavailable, then a survey may be used to identify patients at higher risk for CIN
than the general population. |
Consensus Statement 4
In the setting of emergency procedures, where the benefit of very early imaging outweighs the risk of waiting, the procedure can be performed
without knowledge of serum creatinine or eGFR. |
Consensus Statement 5
The presence of multiple CIN risk factors in the same patient or high risk clinical scenarios can create a very high risk (~50%) for CIN and (~15%)
acute renal failure requiring dialysis after contrast exposure. |
Consensus Statement 6
In patients at increased risk for CIN undergoing intra-arterial administration of contrast, ionic high-osmolality agents pose a greater risk for CIN
than low-osmolality agents. Current evidence suggests that no contrast media present a lower risk for CIN than non-ionic isosmolar contrast. |
Consensus Statement 7
Higher contrast volumes (>100 ml) are associated with higher rates of CIN in patients at risk. However, even small (~30 ml) volumes of iodinated
contrast in very high risk patients can cause CIN and acute renal failure requiring dialysis, suggesting the absence of a threshold effect. |
Consensus Statement 8
Intra-arterial administration of iodinated contrast appears to pose a greater risk of CIN above that with intravenous administration. |
Consensus Statement 9
Adequate intravenous volume expansion with isotonic crystalloid (1.0-1.5 ml/kg/h) for 3-12 hours before the procedure and continued for
6-24 hours afterwards can lessen the probability of CIN in patients at risk. The data on oral as opposed to intravenous volume expansion as a
CIN prevention measure are insufficient. |
Consensus Statement 10
No adjunctive medical or mechanical treatment has been proven to be efficacious in reducing the risk of CIN. Prophylactic haemodialysis or
haemofiltration has not been validated as an effective strategy. |
| Table 1. Consensus statements, adapted from McCullough et al, 2006.12 |
eGFR = estimated glomerular filtration rate; CIN = contrast-induced nephropathy; NSAID = nonsteroidal anti-inflammatory drug; Cr = creatinine;
PGE1 = prostaglandin E1
† Volume expansion consisting of intravenous isotonic crystalloid 1-1.5 ml/kg per hr should be given 3-12 hours before and 6-24 hours after the
procedure. †† Consider potentially beneficial agents such as theophylline, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins),
ascorbic acid (vitamin C), prostaglandin E1 (none approved for this indication). ††† Plans should be made in case contrast induced nephropathy (CIN)
occurs and dialysis is required. * Adapted from McCullough et al, 200612
Figure 1. Algorithm for management of patients receiving iodinated contrast media.12 |
The best indication of the healthcare impact of CIN comes
from large studies of hospital patients. The frequency of
CIN has decreased over the past decade from a general
incidence of ~15% to ~7% of patients receiving iodinated
contrast,14 due to a greater awareness of the problem,
better risk prevention measures, and improved iodinated
contrast media with less renal toxicity. However, many
cases of CIN continue to occur because of the everincreasing
numbers of procedures requiring contrast
medium. Nash et al reported that radiographic contrast
media were the third commonest cause of hospitalacquired
renal failure (after decreased renal perfusion and
nephrotoxic medications) and were responsible for 11%
of cases.3 The mortality rate in cases of CIN was 14%.
The proportion of cases of hospital-acquired renal failure
attributed to contrast media (11%) was almost identical
to an earlier series.15 However, in the more recent study,
there were more cases following cardiac procedures and
fewer after non-cardiac angiography.
Using a CIN definition of a 25% rise in serum creatinine,
it has been suggested that in the past the frequency
of CIN after use of contrast media in an unselected
group of cardiology patients may be up to 15%.16,17 In
patients with impaired renal function at baseline the
risk is considerably higher and the significance of renal
impairment as a risk marker is reviewed later in this paper.
It has been recognised for some time that the risk of
death is increased in patients developing acute kidney
injury after contrast medium administration. In a large
retrospective study of over 16,000 hospital in-patients
undergoing procedures requiring contrast medium, a
total of 183 subjects developed CIN (defined as a 25%
increase in serum creatinine).18 The risk of death during
hospitalisation was 34% in subjects who developed CIN
compared with 7% in matched controls who had received
contrast medium but did not develop CIN. Even after
adjusting for comorbid disease, patients with CIN had
a 5.5-fold increased risk of death.18 The high risk of inhospital
death associated with CIN was also documented
in a retrospective analysis of 7586 patients, of whom
3.3% developed CIN after exposure to contrast medium.
Among the patients who developed CIN, the in-hospital
death rate was 22% compared with only 1.4% in patients
who did not develop ARF.19 The mortality rates at
1 year after development of CIN (12.1%) and at 5 years
(44.6%), were higher compared to rates of 3.7% and
14.5% respectively in patients who did not develop CIN (p<0.001), indicating that the increased risk of death
persisted in the long term. A further study confirmed the
high mortality in patients who develop CIN, especially
in those who require dialysis: the hospital mortality
was 7.1% in CIN patients and 35.7% in patients who
required dialysis. By 2 years, the mortality rate in patients
who required dialysis was 81.2%.16 CIN (defined as an
increase =25% in serum creatinine) occurred in 37%
of 439 patients with renal impairment (baseline serum
creatinine 1.8 mg/dl) undergoing PCI.20 In this group,
the hospital mortality rate was 14.9% compared with
4.9% in patients without CIN (p=0.001). The cumulative
1-year mortality rates were 37.7% and 19.4% respectively.
The 1-year mortality was 45.2% for patients with CIN
requiring dialysis and 35.4% for those with CIN not
requiring dialysis.20 In patients undergoing primary PCI
for MI, short and long-term mortality rates were also
significantly higher in those who developed CIN.21,22
In PCI patients, it has been shown that CIN is an
independent predictor of mortality.23
Impact of CIN on clinical course and outcome
As well as an increased risk of death, CIN is also
associated with other adverse outcomes including late
cardiovascular events. In one registry series of 5967 PCI
patients, the development of CIN was associated with an
increased incidence of myocardial infarction and target
vessel revascularisation at 1 year.23 Another large PCI
study documented the link between contrast-induced
rises in serum creatinine, post-procedural increases in
creatinine kinase MB sub-fraction (CK-MB), and the
risk of late cardiovascular events.24 In a group of 5397
patients, a postprocedural rise in serum creatinine was a
more powerful predictor of late mortality than CK-MB.
Creatinine increases were associated with a 16% rate of
death or myocardial infarction at 1 year, rising to 26.3%
when CK-MB levels were also elevated.24
More in-hospital events such as bypass surgery,
bleeding requiring transfusion and vascular
complications were observed in patients who developed
CIN, both in those with previous renal dysfunction
and those with previously normal renal function. At
one year, the cumulative rate of major adverse cardiac
events (MACE) was significantly higher in patients who
had developed CIN (p<0.0001 for patients with and
without chronic kidney disease).25 However, others have
observed no difference in the rates of MI and target
vessel revascularisation in patients with CIN.20
The development of CIN has also been associated
with an increased hospital stay. In one series, the postprocedure hospital stay was longer in patients who
developed CIN, regardless of baseline renal function.25
In a series of 200 patients undergoing PCI for acute
myocardial infarction, patients who developed CIN had a
longer hospital stay, a more complicated clinical course
and a significantly increased risk of death compared to
those without CIN.22
Risk of CIN requiring dialysis
While most cases of CIN reflect mild transient
impairment of renal function, dialysis is needed in a small
proportion of patients. The literature review conducted
by the CIN Consensus Working Panel suggests that the
need for dialysis after CIN varies according to patients
underlying risks at the time of contrast administration
but is generally less than 1%,16,26,27 although it was
considerably higher in some older studies with HOCM.28,29 In contemporary studies, CIN requiring dialysis developed
in 3.1% of patients with underlying renal impairment30 and 3% of patients undergoing primary PCI for MI.22 Although CIN requiring dialysis is relatively rare, the
impact on patient prognosis is considerable, with high
hospital and 1-year mortality rates.16,20
Pathophysiology of CIN
The CIN Consensus Working Panel reviewed the
pathophysiology of CIN and agreed that it certainly
involves the interplay of multiple factors. These include
vasoconstriction, impaired vasodilation, oxidative stress
and direct tubular toxicity, all contributing to medullary
hypoxia. A detailed review of pathophysiology is outside
the scope of this paper and the reader is referred to the
published review for further information.10
The role of baseline renal function screening
Virtually every report describing risk factors for CIN
lists abnormal baseline serum creatinine, low GFR or
underlying renal disease as risk factors and almost
every multivariate analysis has shown that pre-existing
renal impairment is an independent risk predictor for
CIN.14,16,19,26,31,32 The consensus view of the group, after
reviewing the published data, was that the risk of CIN
is increased in patients with an estimated glomerular
filtration rate (eGFR) <60 ml/minute (equivalent to
serum creatinine of =1.3 mg/dl [=114.9 µmol/l] in men
and =1.0 mg/dl [=88.4 µmol/l] in women) and that
special precautions should be taken in these patients.
Measurement of baseline renal function
It is important to assess renal function before
administration of contrast medium to ensure that
appropriate steps are taken to reduce the risk. Since
serum creatinine alone does not provide a reliable measure of renal function, the National Kidney
Foundation Kidney Disease Outcome Quality Initiative
(K/DOQI) recommends that clinicians should use an
eGFR calculated from the serum creatinine as an index
of renal function rather than using serum creatinine.33
The CIN Consensus Working Panel agreed that eGFR
should be determined prior to contrast administration,
using the abbreviated Modification of Diet in Renal
Disease (MDRD) formula.
Use of surveys/questionnaires
It is highly desirable to have an eGFR value (calculated
from a recent serum creatinine measurement) available
in order to assess the risk of CIN, but this may be
impractical in some circumstances. Where renal function
data are unavailable, a simple survey or questionnaire
may be used to identify patients at higher risk for
CIN than the general population in whom appropriate
precautions should be taken to reduce the risk of CIN.34-36
Emergency situations
In the setting of emergency procedures, where the
benefit of very early imaging outweighs the risk
of waiting for the results of a blood test, it may
be necessary to proceed without serum creatinine
assessment or GFR estimation.7 However, where
possible, an indication should be obtained of the
likelihood that the patient has impaired renal function
that may increase the risk of CIN, to enable suitable
precautions to be taken.
Risk markers for CIN
The panel preferred the use of the term risk marker
to risk factor since many of these indicators are
non-modifiable patient characteristics that are not
necessarily directly causative. The most important
element of risk stratification is baseline renal filtration
function which is a surrogate for reduced nephron
mass and renal parenchymal function. As already
noted above, abnormal baseline serum creatinine, low
GFR or underlying renal disease are widely reported
as risk factors and almost every multivariate analysis
has shown that pre-existing renal impairment is an
independent risk predictor for CIN.8 The consensus
view of the group, after reviewing the published data,
was that the risk of CIN is increased in patients with
an eGFR <60 ml/minute and that special precautions
should be taken in these patients.
Other risk factors include diabetes mellitus,23,37
volume depletion,38 nephrotoxic drugs, haemodynamic
instability24,39 and other co-morbidities. Importantly
diabetes is neither necessary nor sufficient as a determinant for CIN. However, diabetes appears to
act as a risk multiplier, meaning that in a patient with
CKD it amplifies the risk of CIN. Several large series
of PCI patients have shown an association between
CIN and indicators of haemodynamic instability such
as periprocedural hypotension and use of an intraaortic
balloon pump (IABP).24,25 It is unsurprising that
hypotension increases the risk of CIN since it increases
the likelihood of renal ischemia and is a significant
risk factor for acute renal failure in acutely ill patients.
Anaemia has also been reported as a predictor of CIN.40
The effect of risk factors is additive and the likelihood
of CIN rises sharply as the number of risk factors
increases.16,39 A similar pattern of additive risk has been
documented for nephropathy requiring dialysis.26
The additive nature of risk has allowed the development
of prognostic scoring schemes,14,39 but since none of
the published schemes has been adequately studied or
prospectively validated in different populations, it is not
appropriate to recommend routine use of any particular
risk scoring in clinical practice. However, the concept is
that in a patient with CKD, DM, and other comorbidities,
predicted risks of CIN can approach ~50% and the risk
of renal failure requiring dialysis ~15%.
High-risk situation and procedures
Many clinical situations may arise in which the risk of
CIN is increased and the CIN Consensus Working Panel
reviewed the published literature.5 However the evidence
is very limited for many situations and in all cases the
decision to administer contrast medium is a matter for
clinical judgment based on the clinical status of the
patient and the expected benefits of the investigation or
procedure. In particular there was insufficient evidence
to make definitive statements about the risk of CIN in
patients undergoing coronary artery bypass surgery after
contrast exposure or in patients with cirrhosis (although
cirrhosis may be a risk factor in patients undergoing
transarterial chemoembolisation). As already noted, in
PCI patients periprocedural haemodynamic instability
may be associated with an increased risk of CIN, but no
published evidence was identified on the significance of
shock or hypotension in other situations. The published
literature on the risk of CIN in renal transplant recipients
is inconsistent.5
Contrast medium use
Choice of contrast medium
There is good evidence that low-osmolar contrast media
(LOCM) are less nephrotoxic than high-osmolar contrast
media (HOCM) in patients at increased risk for CIN.
A meta-analysis published in 1992 evaluated the
relative nephrotoxicity of HOCM and LOCM. The pooled
odds ratio for the prevalence of CIN events (rise in
serum creatinine of >44.2 µmol/l (>0.5 mg/dl)) in 25
trials was 0.61 (95% confidence interval (CI) 0.48-0.77),
indicating a significant reduction in risk with LOCM.41
Studies published since this meta-analysis generally
support these findings.42
Most studies comparing different LOCM have been
small trials that have not shown clinically relevant
variation between the renal effects of different LOCM
and there is insufficient evidence to draw definitive
conclusions about possible differences.6
The available evidence supports the conclusion that no
contrast medium is associated with a lower risk of CIN
than isosmolar contrast medium (IOCM). In a prospective
randomised double-blind trial in diabetic patients with
renal impairment undergoing coronary or aortofemoral
angiography, the mean peak increase in serum creatinine
was significantly less in the iodixanol group than in
the iohexol group (p=0.001). Using the most common
definition of CIN (an increase of 0.5 mg/dl (44.2 µmol/l)
in serum creatinine), CIN occurred in 2 of 64 patients
(3%) in the iodixanol group and 17 of 65 (26%) in the
iohexol group (p=0.002).43 The results of a prospective
open-label comparison of iodixanol and iohexol were
consistent with a lower incidence of CIN with iodixanol.44
A systematic review by Solomon was also
consistent with a low rate of contrast nephropathy
with iodixanol.45 A total of 17 prospective clinical trials
(1365 patients) were included, but only two of these
trials were randomised comparisons of LOCM and IOCM
and the other data came from the placebo arms of
13 trials of preventive strategies for CIN and the LOCM
arms of 2 trials comparing LOCM and HOCM. Finally, a
meta-analysis of the renal tolerability of another IOCM,
iotrolan 280, provides further evidence that IOCM are
associated with a lower risk of post-procedure renal
impairment.46 In an analysis of 14 double-blind studies,
it was found that iotrolan had less effect on renal
function than the LOCM with which it was compared
(iopamidol, iohexol, iopromide).
On the basis of these results, the CIN Consensus
Working Panel concluded that in patients with CKD
and particularly those with DM undergoing angiographic
procedures, current evidence suggests no contrast
medium presents a lower risk for CIN than nonionic,
iso-osmolar contrast. This consensus view was
incorporated in an algorithm for patient management which indicates that in patients with CKD (eGFR
<60 ml/min/1.73 m2), the choice of iodinated contrast
medium should be considered.
Volume of contrast
Numerous studies have shown that the volume of
contrast medium is a risk factor for CIN and that
the mean contrast volume is higher in patients with
CIN, and most multivariate analyses have shown
that contrast volume is an independent predictor of
CIN.16,23,26,39 However, even small volumes (~30 ml)
of contrast medium can have adverse effects on renal
function in patients at particularly high risk.47
Intra-arterial versus intravenous administration
A number of studies have provided circumstantial
evidence that the risk of CIN may be higher following
intra-arterial administration than after intravenous
injection.48,49 However, none of these studies provides an
insight into the significance of the route of administration
for CIN risk in contemporary practice, especially with
regard to CT studies, when a comparatively large
volume of contrast medium may be given as a compact
intravenous bolus rather than an infusion. The limited
evidence that is available suggests that there is a
significant risk of CIN in these circumstances.50
Other strategies for reducing the risk of CIN
Volume expansion
Volume expansion and treatment of dehydration has
a well established role in reducing the risk of CIN,
although few studies address this theme directly.
There are limited data on the most appropriate choice
of intravenous fluid, but the evidence indicates that
isotonic saline is more effective than half-normal
saline.51 Additional confirmatory trials with sodium
bicarbonate52 are needed.
There is also no clear evidence to guide the choice of
the optimal rate and duration of infusion. However,
good urine output (>150 ml/hr) in the six hours after the procedure has been associated with reduced rates
of CIN in one study.53 Oral volume expansion may have
some benefit, but there is not enough evidence to show
that it is as effective as intravenous volume expansion.54
Dialysis and haemofiltration
Contrast medium is removed by dialysis, but there is
no clinical evidence that prophylactic dialysis reduces
the risk of CIN, even when carried out within 1 hour
or simultaneously with contrast administration.
Haemofiltration performed before and after contrast
deserves further investigation given reports of reduced
mortality and need for haemodialysis,55 but the high
cost and need for ICU admission will also limit the
utility of this prophylactic approach.
Pharmacological strategies
The CIN Consensus Working Panel considered that, of
the pharmacological agents that have been evaluated,
theophylline, statins, ascorbic acid and prostaglandin E1
deserve further evaluation.9 N-acetylcysteine is not
consistently effective in reducing the risk of CIN. Nine
published meta-analyses were identified, all documenting
the significant heterogeneity between studies and pooled
odds ratios for N-acetylcysteine approaching unity.
Fenoldopam, dopamine, calcium channel blockers, atrial
natriuretic peptide and L-arginine have not been shown
to be effective. Furosemide, mannitol and an endothelin
receptor antagonist are potentially detrimental.9
Conclusion
Ten consensus statements and an accompanying
algorithm have been developed. These can be used to
guide the management of patients receiving iodinated
contrast medium. This consensus programme is
important as it is the first attempt to systematically
review all relevant information on CIN, a common
and serious problem. It integrates the viewpoints of
cardiologists, nephrologists and radiologists. Guidelines
and quality programmes can be developed from this
base of work in the future.
References
1. McCullough PA, et al. Contrast-induced nephropathy. Crit Care Clin
2005;21:261280.
2. Gleeson TG, et al. Contrast-induced nephropathy. AJR Am J Roentgenol
2004;183:16731689.
3. Nash K, et al. Hospital-acquired renal insufficiency. Am J Kidney Dis
2002;39:930936.
4. Meguid El Nahas A, et al. Chronic kidney disease: the global challenge.
Lancet 2005;365:331340.
5. Becker CR, et al. High-risk situations and procedures. Am J Cardiol
2006;98:37K41K.
6. Davidson C, et al. Contrast medium use. Am J Cardiol 2006;98:42K58K.
7. Lameire N, et al. Baseline renal function screening. Am J Cardiol
2006;98:21K26K.
8. McCullough PA, et al. Risk prediction of contrast-induced nephropathy.
Am J Cardiol 2006;98:27K36K.
9. Stacul F, et al. Strategies to reduce the risk of contrast-induced
nephropathy. Am J Cardiol 2006;98:59K77K.
10. Tumlin J, et al. Pathophysiology of contrast-induced nephropathy.
Am J Cardiol 2006;98:14K20K.
11. McCullough PA, et al. Epidemiology and prognostic implications of
contrast-induced nephropathy. Am J Cardiol 2006;98:5K13K.
12. McCullough PA, et al. Overview. Am J Cardiol 2006;98:2K4K.
13. Thomsen HS. Guidelines for contrast media from the European
Society of Urogenital Radiology. AJR Am J Roentgenol 2003;181:
14631471.
14. Bartholomew BA, et al. Impact of nephropathy after percutaneous
coronary intervention and a method for risk stratification. Am J Cardiol
2004;93:15151519.
15. Hou SH, et al. Hospital-acquired renal insufficiency: a prospective
study. Am J Med 1983;74:243248.
16. McCullough PA, et al. Acute renal failure after coronary intervention:
incidence, risk factors, and relationship to mortality. Am J Med
1997;103:368375.
17. Iakovou I, et al. Impact of gender on the incidence and outcome
of contrast-induced nephropathy after percutaneous coronary
intervention. J Invasive Cardiol 2003;15:1822.
18. Levy EM, et al. The effect of acute renal failure on mortality. A cohort
analysis. JAMA 1996;275:14891494.
19. Rihal CS, et al. Incidence and prognostic importance of acute
renal failure after percutaneous coronary intervention. Circulation
2002;105:22592264.
20. Gruberg L, et al. The prognostic implications of further renal function
deterioration within 48 h of interventional coronary procedures in
patients with pre-existent chronic renal insufficiency. J Am Coll Cardiol
2000;36:15421548.
21. Sadeghi HM, et al. Impact of renal insufficiency in patients undergoing
primary angioplasty for acute myocardial infarction. Circulation
2003;108:27692775.
22. Marenzi G, et al. Contrast-induced nephropathy in patients undergoing
primary angioplasty for acute myocardial infarction. J Am Coll Cardiol
2004;44:1780-1785.
23. Lindsay J, et al. Percutaneous coronary intervention-associated
nephropathy foreshadows increased risk of late adverse events in
patients with normal baseline serum creatinine. Catheter Cardiovasc
Interv 2003;59:338343.
24. Lindsay J, et al. Causes of acute renal dysfunction after percutaneous
coronary intervention and comparison of late mortality rates with
postprocedure rise of creatinine kinase-MB versus rise of serum
creatinine. Am J Cardiol 2004;94:786789.
25. Dangas G, et al. Contrast-induced nephropathy after percutaneous
coronary interventions in relation to chronic kidney disease and
hemodynamic variables. Am J Cardiol 2005;95:1319.
26. Freeman RV, et al. Nephropathy requiring dialysis after percutaneous
coronary intervention and the critical role of an adjusted contrast
dose. Am J Cardiol 2002;90:10681073.
27. Birck R, et al. Acetylcysteine for prevention of contrast nephropathy:
meta-analysis. Lancet 2003;362:598603.
28. Martin-Paredero V, et al. Risk of renal failure after major angiography.
Arch Surg 1983;118:14171420.
29. Gomes AS, et al. Acute renal dysfunction after major arteriography. AJR
Am J Roentgenol 1985;145:12491253.
30. Nikolsky E, et al. Impact of chronic kidney disease on prognosis of
patients with diabetes mellitus treated with percutaneous coronary
intervention. Am J Cardiol 2004;94:300305.
31. Davidson CJ, et al. Cardiovascular and renal toxicity of a nonionic
radiographic contrast agent after cardiac catheterization. A prospective
trial. Ann Intern Med 1989;110:119124.
32. Nikolsky E, et al. Impact of chronic kidney disease on prognosis of
patients with diabetes mellitus treated with percutaneous coronary
intervention. Am J Cardiol 2004;94:300305.
33. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation,
classification, and stratification. Am J Kidney Dis 2002;39:S1266.
34. Tippins RB, et al. Are screening serum creatinine levels necessary prior
to outpatient CT examinations? Radiology 2000;216:481484.
35. Choyke PL, et al. Determination of serum creatinine prior to iodinated
contrast media: is it necessary in all patients? Tech Urol 1998;4:6569.
36. Olsen JC, et al. Utility of the creatinine prior to intravenous contrast
studies in the emergency department. J Emerg Med 1996;14:543546.
37. Dangas G, et al. Contrast-induced nephropathy after percutaneous
coronary interventions in relation to chronic kidney disease and
hemodynamic variables. Am J Cardiol 2005;95:1319.
38. Krumlovsky FA, et al. Acute renal failure. Association with administration
of radiographic contrast material. JAMA 1978;239:125127.
39. Mehran R, et al. A simple risk score for prediction of contrast-induced
nephropathy after percutaneous coronary intervention: development
and initial validation. J Am Coll Cardiol 2004;44:13931399.
40. Nikolsky E, et al. Low hematocrit predicts contrast-induced
nephropathy after percutaneous coronary interventions. Kidney Int
2005;6:706713.
41. Barrett BJ, et al. Metaanalysis of the relative nephrotoxicity of
high- and low- osmolality iodinated contrast media. Radiology
1993;188:171178.
42. Rudnick MR, et al. Nephrotoxicity of ionic and nonionic contrast
media in 1196 patients: a randomized trial. The Iohexol Cooperative
Study. Kidney Int 1995;47:254261.
43. Aspelin P, et al. Nephrotoxic effects in high-risk patients undergoing
angiography. N Engl J Med 2003;348:491499.
44. Chalmers N, et al. Comparison of iodixanol and iohexol in renal
impairment. Br J Radiol 1999;72:701703.
45. Solomon R. The role of osmolality in the incidence of contrast-induced
nephropathy: a systematic review of angiographic contrast media in
high risk patients. Kidney Int 2005;68:22562263.
46. Clauss W, et al. Renal tolerance of iotrolan 280 a meta analysis of 14
double-blind studies. Eur Radiol 1995;5:S7984.
47. Manske CL, et al. Contrast nephropathy in azotemic diabetic patients
undergoing coronary angiography. Am J Med 1990;89:615620.
48. Campbell DR, et al. A comparative study of the nephrotoxicity of
iohexol, iopamidol and ioxaglate in peripheral angiography. Can Assoc
Radiol J 1990;41:133137.
49. Moore RD, et al. Nephrotoxicity of high-osmolality versus lowosmolality
contrast media: randomized clinical trial. Radiology
1992;182:649655.
50. Tepel M, et al. Prevention of radiographic-contrast-agent-induced
reductions in renal function by acetylcysteine. N Engl J Med
2000;343:180184.
51. Mueller C, Buerkle G, Buettner HJ, et al. Prevention of contrast mediaassociated
nephropathy: randomized comparison of 2 hydration
regimens in 1620 patients undergoing coronary angioplasty. Arch
Intern Med 2002;162:329336.
52. Merten GJ, et al. Prevention of contrast-induced nephropathy
with sodium bicarbonate: a randomized controlled trial. JAMA
2004;291:23282334.
53. Stevens MA, et al. A prospective randomized trial of prevention
measures in patients at high risk for contrast nephropathy: Results of
the P.R.I.N.C.E. study. J Am Coll Cardiol 1999;33:403411.
54. Taylor AJ, et al. PREPARED: Preparation for Angiography in Renal
Dysfunction: a randomized trial of inpatient vs outpatient hydration
protocols for cardiac catheterization in mild-to-moderate renal
dysfunction. Chest 1998;114:15701574.
55. Marenzi G, et al. The prevention of radiocontrast-agent-induced
nephropathy by hemofiltration. N Engl J Med 2003;349:13331340. |
|
|
