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 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