HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) All Versions of this Article: CJN.03470708v1 3/5/1242    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Solomon, R. Search for Related Content PubMed PubMed Citation Articles by Solomon, R. Related Collections Related Article

Contrast-Induced Acute Kidney Injury: Is There a Risk after Intravenous Contrast?

Fletcher Allen Health Care, University of Vermont School of Medicine, Burlington, Vermont

Correspondence: Dr. Richard Solomon, UHC 2309, 1 South Prospect Street, Burlington, VT 05401. Phone: 802-847-5030; Fax: 802-847-3607; E-mail: richard.solomon{at}vtmednet.org

	Introduction

Top Introduction Disclosures References

 
Contrast-induced nephropathy (CIN) is a form of acute kidney injury (AKI) that follows exposure to intravascular contrast media. Its pathogenesis involves renal ischemia, particularly in the outer medulla, where oxygen delivery is already at critical levels, and direct epithelial cell toxicity. There is no consensus regarding the definition of CIN. Changes in serum creatinine (a marker of glomerular filtration rather than injury) are the most widely used, but different definitions (e.g., 0.5 mg/dl or 25% increase) are often used in clinical trials. These definitions have been validated as surrogate markers because those who experience changes of this magnitude have a significant increase in short- and long-term morbidity and mortality. This association between CIN and long-term adverse outcomes has been best demonstrated by retrospective analyses of cardiac angiography cohorts (1–3); however, 90% of contrast media are used for computed tomography (CT) imaging, and patients who undergo contrast-enhanced CT may differ significantly from those who undergo angiography.

First, less contrast medium is given during a contrast-enhanced CT scan than is usually used in cardiac angiography, particularly when an intervention is performed. Second, more advanced vascular disease (e.g., diabetes, hypertension) and hemodynamic instability are usually present in the cardiac angiography cohort than in a CT population. Finally, the administration of contrast media intra-arterially may be associated with atheromatous emboli. For these reasons, the incidence of CIN is often considered to be higher in the cardiac population.

Using a prospective design, routine repeat serum creatinine determinations 48 to 72 h after contrast, six definitions of contrast-induced AKI (CI-AKI), and the electronic medical record of the VA health care system, Weisbord et al. (4) were able to determine the incidence of CIN and its long-term consequences in a group of patients who received intravenous contrast media for CT imaging. The minority of patients received any prophylaxis, in the form of intravenous saline before and/or after contrast exposure, use of N-acetylcysteine, or advice regarding discontinuation of nephrotoxins. What does their observational study tell us?

First, they restrict their analyses to individuals with an estimated GFR (by Modification of Diet in Renal Disease [MDRD]) of <60 ml/min per 1.73 m². As expected, the incidence of CI-AKI varied with the definition used, from 0 to 11%. Furthermore, the incidence of CI-AKI (defined as an increase in creatinine of 0.5 mg/dl or 25%) increased two- to four-fold, respectively, as kidney function decreased from 45 to 60 to <45 ml/min per 1.73 m². A novel finding was that the incidence was much higher in inpatients compared with outpatients, although this effect was mitigated at the lower GFR range. Use of prophylaxis was not associated with a lower incidence of CI-AKI.

What do these observations mean for the treatment of patients who have kidney disease and undergo contrast-enhanced CT procedures? For outpatients, the risk for CI-AKI, particularly in patients with estimated GFR (eGFR) >45 ml/min per 1.73 m², is extremely low (approximately 2%). These patients do well even in the absence of prophylaxis. Conclusions that are consistent with this were reached in a systematic review of intravenous contrast by Katzberg and Barrett (5). In addition, three recent prospective, randomized trials involving contrast-enhanced CT in patients with eGFR <60 ml/min per 1.73 m²—IMPACT (Isovue-370 and Visipaque-320 in renally impaired patients undergoing computed tomography) (6), ACTIVE (Abdominal computed tomography: Iomeron-400 versus Visipaque-320 enhancement study) (7), and PREDICT (Patients with renal impairment and diabetes undergoing computed tomography) (8)—found an overall incidence of CI-AKI (defined as a 25% increase in creatinine) of approximately 5%. The majority of the patients did not receive any intravenous fluid administration or pharmacologic prophylaxis. For hospitalized patients and/or those with eGFR <45 ml/min per 1.73 m², the incidence of CI-AKI was significantly higher in the cohort described by Weisbord et al. Whether prophylaxis is efficacious in these patients is not addressed in the article. It would nevertheless seem that prophylaxis is unnecessary for outpatients with eGFR >45 ml/min per 1.73 m² and should be considered for inpatients and for outpatients with an eGFR <45 ml/min per 1.73 m².

What about the relationship of CI-AKI to long-term adverse outcomes? Are the worse outcomes that are seen with coronary administration of contrast also seen with intravenous contrast administration? A clear trend toward worse outcomes was seen by Weisbord et al., although this did not reach statistical significance. It is likely that too few adverse events occurred in this population, reducing the statistical power; however, a retrospective review by Levy et al. (9) involving more than 16,000 contrast administrations of which 48% involved contrast-enhanced CT did find an association with hospital mortality.

Although the incidence of CI-AKI may be less with intravenous contrast administration, the widespread and increasing use of contrast-enhanced CT examinations still leaves a sizable population vulnerable to this event. The threshold for high risk for CI-AKI is shifted toward a lower eGFR because of the smaller dosage of contrast administered. It is the amount of contrast agent per nephron that is the best metric for contrast dosage, and this is approximated by mgI/eGFR (10). Further clinical trials are necessary to determine whether prophylaxis in this high-risk group is efficacious.

	Disclosures

Top Introduction Disclosures References

 
None.

	Footnotes

 
Published online ahead of print. Publication date available at www.cjasn.org.

See related article, "Incidence and Outcomes of Contrast-Induced AKI Following Computed Tomography," on pages 1274–1281.

	References

Top Introduction Disclosures References

 

1. Rihal CS, Textor SC, Grill DE, Berger PB, Ting HH, Best PJ, Singh M, Bell MR, Barsness GW, Mathew V, Garratt KN, Holmes DR Jr: Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation105 :2259 –2264,2002[Abstract/Free Full Text]
2. Gruberg L, Mintz GS, Mehran R, Gangas G, Lansky AJ, Kent KM, Pichard AD, Satler LF, Leon MB: The prognostic implications of further renal function deterioration within 48 h of interventional coronary procedures in patients with pre-existent chronic renal insufficiency. J Am Coll Cardiol36 :1542 –1548,2000[Abstract/Free Full Text]
3. McCullough PA, Wolyn R, Rocher LL, Levin RN, O'Neill WW: Acute renal failure after coronary intervention: Incidence, risk factors, and relationship to mortality. Am J Med103 :368 –375,1997[CrossRef][Medline]
4. Weisbord SD, Mor MK, Resnick AL, Hartwig KC, Palevsky PM, Fine MJ: Incidence and outcomes of contrast-induced AKI following computed tomography. Clin J Am Soc Nephrol3 :1274 –1281,2008[Abstract/Free Full Text]
5. Katzberg RW, Barrett BJ: Risk of iodinated contrast material-induced nephropathy with intravenous administration. Radiology243 :622 –628,2007[Free Full Text]
6. Barrett B, Thomsen H, Katzberg R: Nephrotoxicity of low-osmolar iopamidol vs iso-osmolar iodixanol in renally impaired patients: The IMPACT study. Invest Radiol41 :815 –821,2006[CrossRef][Medline]
7. Thomsen HS, Morcos SK, Erley CM, Grazioli L, Bonomo L, Ni Z, Romano L, Investigators in the Abdominal Computed Tomography: The ACTIVE trial: Comparison of the effects on renal function of iomeprol-400 and iodixanol-320 in patients with chronic kidney disease undergoing abdominal computed tomography. Invest Radiol43 :170 –178,2008[Medline]
8. Kuhn M, Chen N, Sahani DV, Reimer D, van Beek EJ, Heiken JP, So GJ: The PREDICT study: A randomized double-blind comparison of contrast-induced nephropathy after low- or isoosmolar contrast agent exposure. Am J Radiol191 :151 –157,2008[Abstract/Free Full Text]
9. Levy EM, Viscoli CM, Horwitz RI: The effect of acute renal failure on mortality: A cohort analysis. JAMA275 :1489 –1494,1996[Abstract/Free Full Text]
10. Sherwin PF, Cambron R, Johnson JA, Pierro JA: Contrast dose-to-creatinine clearance ratio as a potential indicator of risk for radiocontrast-induced nephropathy: Correlation of D/CrCl with area under the contrast concentration-time curve using iodixanol. Invest Radiol40 :598 –603,2005[CrossRef][Medline]

This Article Full Text (PDF) All Versions of this Article: CJN.03470708v1 3/5/1242    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Solomon, R. Search for Related Content PubMed PubMed Citation Articles by Solomon, R. Related Collections Related Article