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Post PCI Contrast Induced Nephropathy

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... 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 ... – PowerPoint PPT presentation

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Title: Post PCI Contrast Induced Nephropathy


1
Post PCI Contrast Induced Nephropathy
  • Brandon M. Williams M.D.
  • A.M. Report 9/9/08

2
Acute Renal Failure Post Cath/PCI
  • Renal atheroemboli
  • Hemodynamic instability with decreased renal
    perfusion
  • Contrast induced nephropathy

3
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

4
Evidence of Renal Atheroemboli
5
Renal Hypoperfusion
  • Oliguria/anuria
  • Postischemic acute tubular necrosis (increasing
    Cr, normal to reduced uop, granular casts, FeNa gt
    1

6
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 gt25 or absolute increase of
    gt0.5mg/dl

7
CIN Timeline
  • Symptoms initially seen 24-48 hours after
    exposure
  • Cr peaks at 5-7 days
  • Normalizes usually within 7-10 days

Mehran, 2007
8
CIN Incidence
  • 3rd most common hospital acquired renal failure
  • gt5 of patients with cath experience transient
    increase Cr gt 1.0 from baseline

Up to Date Complications of diagnostic cardiac
catheterization
9
Outcomes of CIN
  • Prognosis of patients with CIN significantly
    worse than those without
  • Case control study 1600 pts with contrast,
    mortality rate with CIN (n183) 5.5 times of
    matched controls (n174)
  • Increased risk of mortality if require
    hemodialysis
  • Increase in cost of 10,345 for hospital stay

10
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

11
Patient CIN Risk Factors
  • RENAL INSUFFICIENCY
  • DIABETES MELLITUS WITH CRI
  • Volume depletion
  • Age gt 75
  • Hypotension
  • CHF
  • Other renal toxins
  • Renal transplant
  • Hypoalbuminemia

12
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

13
Pathogenesis of CIN
  • In animal models, some evidence of ATN but
    mechanism is not fully understood.
  • Theories
  • Renal vasoconstriction
  • Cytotoxic effect of contrast agent

14
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)

15
Vasa Recta
16
Direct Tubular Injury
  • Direct cytotoxic effects
  • Oxygen free radicals

17
McCullough et al.
18
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

19
McCullough et al.
20
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

21
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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