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8/6/2019 20060828 Constrast nephropathy
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Prophylaxis Strategies for Contrast-
Induced Nephropathy
JAMA. 2006;295:2765-2779
Neesh Pannu, MD; Natasha Wiebe, MMath,Pstat; Marcello Tonelli, MD, SM
for the Alberta Kidney Disease Network
,
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Contrast-Induced Nephropathy
3rd leading cause of hospital-acquired ARF (12%)
Significant consequencesProlonged hospitalization
Requirement for dialysis
Increased risk of death
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Contrast-Induced Nephropathy
ARF in cardiac catheterization
In-hospital mortality: 20% in unselected patients1-year mortality: 66% in AMI & preexisting renal
dysfunction
Review
Strategies to prevent (evidence-based)
Key areas of future research
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METHODS
English language
MEDLINE & EMBASE 1966 to January 2006
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Risk Factors
Radio contrast nephropathy, contrastmedia,
risk, diabetes, nephrotoxicity, creatinine,coronary disease, coronary procedures,
dehydration, and hypovolemia
59 studies
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Clinical Trial
Radio contrast nephropathy, phropathy, contrast
media, acetylcysteine, theophylline, sodiumbicarbonate, HMG Co-A reductase inhibitors,
ascorbic acid, kidney diseases, renal
insufficiency, kidney failure, nephropathy,
fenoldopam, saline, and diuretics
331 studies, 63 randomized controlled trials
(RCT)
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DEFINITIONS AND EPIDEMIOLOGY
No universally accepted definition
Absence of other identifiable causes25% elevation in serum creatinine
Absolute increase of 0.5 mg/dl (44 mol/L), 2 to 7 days
later
Adverse short- and long-term outcomes
Unclear causal pathway to adverse cardiovascular
outcome
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DEFINITIONS AND EPIDEMIOLOGY
Incidence: 1.6% ~ 2.3%
Intra-arterial > intra-venous adminstrationLower as defined with absolute increase
Lower as earlier SCr measurement
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Contrast Nephropathy
Nonoliguric & reversible
SCr peaks between 2 and 5 days SCr returns to normal within 14 days
Requiring dialysis: 0.4%
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RISK FACTORS
Retrospective, coronary angiography
Periprocedural hydration ?Accurate assessment of comorbidity ?
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Patient-Related Factors
Diabetes & chronic renal disease: 4 fold
Hypovolemia, decreased effective volume Never assessed in clinical trials
Benefit in hydration
Deleterious effect of diuretics
Cardiogenic shock, IABP, hypotension, CHF, EF <40%
Female: not increase risk independently
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Non-Patient-Related Factors
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Non-Patient-Related Factors
Osmolality > 780 mOsm/kg: nephrotoxicity
1992 meta-analysis in 25 randomized trials>1400 mOsm/kg in prezxisting renal disease:
significantly increase
Iohexol v.s. iopamidol v.s. Iodixanol
25% v.s. 13.5% v.s. 11%
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Non-Patient-Related Factors
Nonionic contrast
ControversialConfounded by differences in osmolality
Several randomized studies: no difference
One post-hoc analysis In preexisting renal dysfunction
Nonionic is better
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RISK STRATIFICATION
None
Validated prospectively or in other databaseComorbidity
Prophylactic interventions
Coronary angiography
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RISK STRATIFICATION Bartholomew (n=20,479), Cr greater than 1 mg/dl
Creatinine clearance < 60 mL/min
IABP
Urgent coronary procedure
Diabetes
CHF
Hypertension Peripheral vascular disease
Contrast volume
2% v.s 28% in nephropathy; 17% risk of death
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RISK STRATIFICATION
Mehran
Older agePresence of hypotension
Anemia
Change in SCr 25% or 0.5 mg/dl
Incidence: 13.1%
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PROPHYLACTIC STRATEGIES
Mechanism: poorly understood
Reduction in renal perfusionDirect tubular toxicity
Limited success in treatment
Renal vasoconstriction
Hypoxia-induced oxidative stress
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PROPHYLACTIC STRATEGIES
Small
Unpowered to detect a significant benefit Not double-blinded
Loss to follow up
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Hydration
No RCT studied hydration alone
10 studies: hydration protocol & diuretics4 forced diuretics with hydration
3 significant increase in nephropathy
2 bolus infusions of N/S 250-300 ml immediately
before or during v.s. slowly infusion for 12 hours
No significant difference
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Hydration
2 Oral hydration v.s prolonged infusion (12 hrs)
Contradictory resultTime, route, fluid tonicity & composition
Isotonic better than hypotonic
Sodium bicarbonate
Alkalinizing tubular fluid and minimizing damage
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Hydration
Suggestive, but incomplete evidence
QuestionAll patients
Route, type, volume, timing
Outpatient ?
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Vasodilators
4 RCTs ³renal dose´ dopamine
None showed a benefit Fenoldopam
Dopamine-1 receptor
Vasodilatory
3 RCTs, 1 favored but not significant
Insufficient vasodilation ??
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Theophylline
9 trials
RR: 0.07 ~ 1.7 (median: 0.25)3 of 5 favored, 1 significant
Change in SCr: -0.29 to 0 mg/dl (median: -0.14)
6/8 favored, 2 significant
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Antioxidants
N-Acetylcysteine
Scavenging oxygen free radicalsEnhancing vasodilatory effect of NO
22 trials
RR: 0.11 to 1.5 (median, 0.72)
11/20 nephropathy, 13/20 change in SCr: favored
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Ascorbic Acid
A double-blinded RCT
23
1 underwent coronary catheterizationOdd ratio: 0.38; 95% CI: 0.17 ~ 0.85
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Extracorporeal Removal of Contrast
4 small trials with impaired renal function
2 no benefit, 1 harmfulCompared with hydration alone in renal
dysfunction
2 trails: benefit
Cost-effective: SCr> 265 umol/L
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SUGGESTED MANAGEMENT STRATEGY
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Conclusion
While several risk factors for contrast-induced
nephropathy have been identified, the development
of an effective prophylaxis strategy for contrast-
induced nephropathy has been limited by our poor
understanding of the pathophysiology and the
clinical significance of this condition. Future research
should focus on correctly identifying higher-risk
patients and testing therapies in the setting of large
well-powered clinical trials.