9.9.08 williams. contrast-induced nephropathy
TRANSCRIPT
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Post PCI Contrast InducedNephropathy
Brandon M. Williams M.D.
A.M. Report 9/9/08
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Acute Renal Failure Post Cath/PCI
Renal atheroemboli
Hemodynamic instability with decreasedrenal perfusion
Contrast induced nephropathy
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Renal Atheroemboli
Other signs of embolization (blue toes,livedo reticularis, Hollenhorst plaques,abdominal pain)
Transient eosinophilia andhypocomplementemia
Renal failure which persists greater than 7days
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Evidence of Renal Atheroemboli
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Renal Hypoperfusion
Oliguria/anuria
Postischemic acute tubular necrosis(increasing Cr, normal to reduced uop,granular casts, FeNa > 1
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Contrast Induced Nephropathy(CIN)
Definition: new-onset or an exacerbationof renal dysfunction after contrastadministration in the absence of othercauses
Cr Increase of >25% or absolute increaseof >0.5mg/dl
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CIN Timeline
Symptoms initially seen 24-48 hours afterexposure
Cr peaks at 5-7 days
Normalizes usually within 7-10 days
Mehran, 2007
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CIN Incidence
3rd most common hospital acquired renalfailure
>5% of patients with cath experiencetransient increase Cr > 1.0 from baseline
Up to Date Complications of diagnostic cardiac catheterization
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Outcomes of CIN
Prognosis of patients with CIN significantlyworse than those without
Case control study 1600 pts with contrast,
mortality rate with CIN (n=183) 5.5 timesof matched controls (n=174)
Increased risk of mortality if require
hemodialysis Increase in cost of $10,345 for hospital
stay
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CIN and Coronary Procedures
Higher mortality than other types of CIN 3% primary PCI for ACS (Marenzi et al 2004)
McCullough et al. 19971800 pts with coronary interventions withcontrast- ARF 14%, dialysis 0.8%
- In house mortality for those to HD 36% (1% forthose without HD)- 2 yr survival 19% in those needing HD
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Patient CIN Risk Factors
RENAL INSUFFICIENCY
DIABETES MELLITUS WITH CRI
Volume depletion
Age > 75 Hypotension
CHF
Other renal toxins Renal transplant
Hypoalbuminemia
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Procedure CIN Risk Factors
Multiple studies in 72 hour period
Intra-arterial injection site
High volume of contrast
High osmolality of contrast1st generation: ionic monomers, 14-18Kmosmol/kg
2nd generation: nonionic monomers, 500-850mosmol/kg3rd generation: nonionic dimers, ~290mosmol/kg
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Pathogenesis of CIN
In animal models, some evidence of ATNbut mechanism is not fully understood.
Theories:
Renal vasoconstriction
Cytotoxic effect of contrast agent
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Renal Vasoconstriction
Contrast induced release of endothelin (?importance) and adenosine
High osmolality of contrast can cause areduction of medullary blood flowsecondary to increased viscosity of theblood flowing through the vasa recta
(usually low viscosity)
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Vasa Recta
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Direct Tubular Injury
Direct cytotoxic effects
Oxygen free radicals
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McCullough et al.
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Prevention
Contrast: low or iso-osmolar (similar results)Omnipaque (iohexol) 844mOsm/kg
Hold nephrotoxic drugs (NSAIDs, calcineurininhibitors, diuretics, aminoglycosides, metformin)
Hydration: NS better than NS, ?sodiumbicarbonate, ascorbic acid, and N-acetylcysteine
Continue statin Hemofiltration (Cr 3-4) 6hr before and 12-18hr
post ? IV antioxidants, renal vasodilators, forced
hydration
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McCullough et al.
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At UNC
Hydration: NS at 1mL/kg/hr for 12 hours prior tocath
Acetylcystein 600-1200mg po BID x 4 doses (2doses the day prior and 2 the day of)
Na Bicarb: 150mEq in 1L D5W at
3mL/kg/hour(max 110kg) x 1 hour on call toprocedure, then 1mL/kg/hour (max 110kg) x 6hours
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References
Marenzi et al. Contrast-induced nephropathy in patients undergoingprimary angioplasty for acute myocardial infarction. J Am CollCardiol, 44, 2004. pp 1780-1785
McCullough et al. Contrast-Induced Acute Kidney Injury. J Am CollCardiol, 51, 2008, 1419-1428
Mehran. Contrast-Induced Nephropathy Remains a Seriouscomplication of PCI. J Interven Cardiol 20. 2007 236-240
Plueger et al. Role of adenosine in contrast media-induced acuterenal failure in diabetes mellitus. Mayo Clin Proc 2000, Dec 70 (12)1275-83
Medic8 Drug Information (omnipaque)
Up to Date Google Images