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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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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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.

20060828 constrast nephropathy

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