9.9.08 williams. contrast-induced nephropathy

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  • 8/2/2019 9.9.08 Williams. Contrast-Induced Nephropathy

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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