ABSTRACTS from 16th International COnference on ... - CRRT Online

Minimizing the Renal Toxicity of Iodinated Contrast
Peter A. McCullough MD, MPH
4:15-4:30
Wednesday, February 15
Educational Objectives:
1) Review the pathophysiology of contrast-induced AKI (CI-AKI)
2) Understand the published data on risk prediction AKI
3) Review the results of major recent trials and meta-analyses on the prevention of CI-AKI
Content Description:
CI-AKI is an important complication after the intravascular administration of iodinated contrast as discussed
above (3,4,6). The definition of CI-AKI implies impairment in renal filtration function occurring within 48 to 72
hours after the procedure, in the absence of alternative etiologies. Past clinical trials have suggested that a rise in
serum creatinine of 0.5 mg/dl or a 25% increase <strong>from</strong> the baseline value indicates occurrence of CI-AKI (5,7).
Serum creatinine concentrations generally peak on day two or three after contrast exposure and typically return
to baseline values within two weeks. (5) In 2007, the Acute Kidney Injury Network proposed the definition to a
rise in serum creatinine ?0.3 mg/dl with oliguria ( 6 hours), which is compatible with the
older definitions. It is expected that in addition to this signal of reduced filtration function, markers of acute
tubular injury in the blood and urine will be used to establish a diagnosis of CI-AKI in the near future.
Future approaches include large planned studies of oral and intravenous antioxidants (including a moderate labile
iron chelator, deferiprone) and intrarenal infusions of renal vasodilators (fenoldopam, natriuretic peptides) using
flow directed catheters. Trials examining the effects of using forced hydration with a balancing pump causing
marked elevations of urine output, thereby reducing the transit time of iodinated contrast in the renal tubules,
will are underway. Novel, hopefully less toxic forms of radio-opaque contrast agents are a source of future interest
and development. The medical community awaits more definitive, unbiased results of future large clinical
trials to help guide safer and more effective strategies for CKD patients at risk for CI-AKI is predictable and is
partially preventable. Reasonable steps should be taken to minimize risk. Novel diagnostic and therapeutic
approaches are needed to manage the ever-increasing numbers of patients undergoing interventions using iodinated
contrast media (48).
Suggested Reading:
McCullough PA, Soman SS: Contrast-induced nephropathy. Crit Care Clin 2005; 21(2):261–280.
2. Brar S: A randomized controlled trial for the prevention of contrast induced nephropathy with sodium bicarbonate
vs. sodium chloride in persons undergoing coronary angiography (the MEENA trial). Abstract 209-9.
Presentation at the 56th Annual Scientific Session of the American College of Cardiology, New Orleans, LA,
USA, 24–27 March 2007.
3. Marenzi G, Lauri G, Campodonico J, Marana I, Assanelli E, De Metrio M, Grazi M, Veglia F, Fabbiocchi F,
Montorsi P, Bartorelli AL. Comparison of two hemofiltration protocols for prevention of contrast-induced
nephropathy in high-risk patients. Am J Med. 2006 Feb;119(2):155-62.
4. Marenzi G, Assanelli E, Marana I, Lauri G, Campodonico J, Grazi M, De Metrio M, Galli S, Fabbiocchi F,
Montorsi P, Veglia F, Bartorelli AL. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty.
N Engl J Med. 2006 Jun 29;354(26):2773-82.
5. Briguori C, Airoldi F, D'Andrea D, et al: Renal insufficiency following contrast media administration Trial
(REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation 2007; 115(10):1211–1217.
6. McCullough PA. Contrast-induced acute kidney injury. J Am Coll Cardiol. 2008 Apr 15;51(15):1419-28.
7. Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, Chavey WE 2nd, Fesmire FM,
Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS, Smith SC Jr, Jacobs AK,
Adams CD, Anderson JL, Antman EM, Halperin JL, Hunt SA, Krumholz HM, Kushner FG, Lytle BW,
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