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Clinical Review
CLINICIAN'S CORNER
JAMA. 2006;295(23):2765-2779. doi: 10.1001/jama.295.23.2765

Prophylaxis Strategies for Contrast-Induced Nephropathy

  1. Neesh Pannu, MD;
  2. Natasha Wiebe, MMath, PStat;
  3. Marcello Tonelli, MD, SM;
  4. for the Alberta Kidney Disease Network
  1. Author Affiliations: Department of Medicine, Division of Nephrology (Drs Pannu and Tonelli and Ms Wiebe), Division of Critical Care (Drs Pannu and Tonelli), and Institute of Health Economics (Dr Tonelli), University of Alberta, Edmonton.
  1. Corresponding Author: Neesh Pannu, MD, 11-107 Clinical Sciences Bldg, 8440-112 St, Edmonton, Alberta, Canada, T6G 2G3 (npannu{at}ualberta.ca).

Abstract

Context  Contrast-induced nephropathy is associated with significant economic and clinical consequences, including prolonged hospitalization, the requirement for dialysis, and an increased risk of death.

Objectives  To summarize the current state of evidence for prophylaxis of contrast-induced nephropathy, provide evidence-based recommendations regarding management of high-risk patients undergoing angiographic procedures, and identify new avenues for research.

Data Sources  Systematic searches of peer-reviewed publications were performed in MEDLINE, EMBASE, and the Cochrane database from 1966 to January 2006. Search terms included radio contrast nephropathy, contrast media, acetylcysteine, theophylline, sodium bicarbonate, HMG Co-A reductase inhibitors, ascorbic acid, kidney diseases, renal insufficiency, kidney failure, nephropathy, fenoldopam, diuretics, and saline or half saline.

Study Selection  Observational studies of risk factors and randomized controlled trials of prophylaxis strategies for contrast-induced nephropathy that specified a definition of contrast-induced nephropathy or postprocedure creatinine level as an outcome measure.

Evidence Synthesis  Important patient-related risk factors for contrast-induced nephropathy include chronic kidney disease, diabetes mellitus, heart failure, older age, anemia, and left ventricular systolic dysfunction. Non–patient-related risk factors include high-osmolar contrast, ionic contrast, contrast viscosity, and contrast volume. Practice guidelines recommend obtaining preprocedural serum creatinine levels among patients with renal disease, diabetes, proteinuria, hypertension, gout, or congestive heart failure. Available evidence, largely based on small- to medium-sized trials, supports the use of hydration, bicarbonate, and low volumes of iso- or low-osmolar contrast in patients at risk. N-acetylcysteine or ascorbic acid may be of value in very high-risk patients.

Conclusions  While several risk factors for contrast-induced nephropathy have been identified, the development of an effective prophylaxis strategy for contrast-induced nephropathy has been limited by our poor understanding of the pathophysiology and the clinical significance of this condition. Future research should focus on correctly identifying higher-risk patients and testing therapies in the setting of large well-powered clinical trials.

For a list of the members of the Alberta Kidney Disease Network, see http://www.akdn.info/rp.html.

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