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Post PCI Contrast Induced Nephropathy

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					Post PCI Contrast Induced
      Nephropathy

   Brandon M. Williams M.D.
      A.M. Report 9/9/08
Acute Renal Failure Post Cath/PCI
• Renal atheroemboli

• Hemodynamic instability with decreased
  renal perfusion

• Contrast induced nephropathy
        Renal Atheroemboli
• Other signs of embolization (blue toes,
  livedo reticularis, Hollenhorst plaques,
  abdominal pain)
• Transient eosinophilia and
  hypocomplementemia
• Renal failure which persists greater than 7
  days
Evidence of Renal Atheroemboli
       Renal Hypoperfusion
• Oliguria/anuria
• Postischemic acute tubular necrosis
  (increasing Cr, normal to reduced uop,
  granular casts, FeNa > 1
   Contrast Induced Nephropathy
               (CIN)
• Definition: “new-onset or an exacerbation
  of renal dysfunction after contrast
  administration in the absence of other
  causes”

• Cr Increase of >25% or absolute increase
  of >0.5mg/dl
               CIN Timeline
• Symptoms initially seen 24-48 hours after
  exposure
• Cr peaks at 5-7 days
• Normalizes usually within 7-10 days




Mehran, 2007
                     CIN Incidence
• 3rd most common hospital acquired renal
  failure
• >5% of patients with cath experience
  transient increase Cr > 1.0 from baseline




Up to Date “Complications of diagnostic cardiac catheterization”
          Outcomes of CIN
• Prognosis of patients with CIN significantly
  worse than those without
• Case control study 1600 pts with contrast,
  mortality rate with CIN (n=183) 5.5 times
  of matched controls (n=174)
• Increased risk of mortality if require
  hemodialysis
• Increase in cost of $10,345 for hospital
  stay
 CIN and Coronary Procedures
• Higher mortality than other types of CIN
• 3% primary PCI for ACS (Marenzi et al 2004)

• McCullough et al. 1997
  1800 pts with coronary interventions with
  contrast
  - ARF 14%, dialysis 0.8%
  - In house mortality for those to HD 36% (1% for
  those without HD)
  - 2 yr survival 19% in those needing HD
       Patient CIN Risk Factors
•   RENAL INSUFFICIENCY
•   DIABETES MELLITUS WITH CRI
•   Volume depletion
•   Age > 75
•   Hypotension
•   CHF
•   Other renal toxins
•   Renal transplant
•   Hypoalbuminemia
     Procedure CIN Risk Factors
•   Multiple studies in 72 hour period
•   Intra-arterial injection site
•   High volume of contrast
•   High osmolality of contrast
    1st generation: ionic monomers, 14-18K
    mosmol/kg
    2nd generation: nonionic monomers, 500-850
    mosmol/kg
    3rd generation: nonionic dimers, ~290
    mosmol/kg
        Pathogenesis of CIN
• In animal models, some evidence of ATN
  but mechanism is not fully understood.

• Theories:
  Renal vasoconstriction
  Cytotoxic effect of contrast agent
      Renal Vasoconstriction
• Contrast induced release of endothelin (?
  importance) and adenosine
• High osmolality of contrast can cause a
  reduction of medullary blood flow
  secondary to increased viscosity of the
  blood flowing through the vasa recta
  (usually low viscosity)
Vasa Recta
        Direct Tubular Injury
• Direct cytotoxic effects
• Oxygen free radicals
McCullough et al.
                 Prevention
• Contrast: low or iso-osmolar (similar results)
  Omnipaque (iohexol) 844mOsm/kg
• Hold nephrotoxic drugs (NSAIDs, calcineurin
  inhibitors, diuretics, aminoglycosides, metformin)
• Hydration: NS better than ½ NS, ?sodium
  bicarbonate, ascorbic acid, and N-acetylcysteine
• Continue statin
• Hemofiltration (Cr 3-4) 6hr before and 12-18hr
  post
• ? IV antioxidants, renal vasodilators, forced
  hydration
McCullough et al.
                   At UNC
• Hydration: NS at 1mL/kg/hr for 12 hours prior to
  cath

• Acetylcystein 600-1200mg po BID x 4 doses (2
  doses 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 to
  procedure, then 1mL/kg/hour (max 110kg) x 6
  hours
                      References
• Marenzi et al. Contrast-induced nephropathy in patients undergoing
  primary angioplasty for acute myocardial infarction. J Am Coll
  Cardiol, 44, 2004. pp 1780-1785
• McCullough et al. Contrast-Induced Acute Kidney Injury. J Am Coll
  Cardiol, 51, 2008, 1419-1428
• Mehran. Contrast-Induced Nephropathy Remains a Serious
  complication of PCI. J Interven Cardiol 20. 2007 236-240
• Plueger et al. Role of adenosine in contrast media-induced acute
  renal failure in diabetes mellitus. Mayo Clin Proc 2000, Dec 70 (12)
  1275-83
• Medic8 Drug Information (omnipaque)
• Up to Date
• Google Images

				
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posted:12/28/2011
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