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The Effect of Renin-Angiotensin-Aldosterone System Blockade on Contrast-Induced Acute Kidney Injury: A Propensity-Matched Study

Authors
Rim, Min YoungRo, HanKang, Woong CholKim, Ae JinPark, HyeonsuChang, Jae HyunLee, Hyun HeeChung, WookyungJung, Ji Yong
Issue Date
Oct-2012
Publisher
W B SAUNDERS CO-ELSEVIER INC
Keywords
Contrast-induced acute kidney injury (AKI); angiotensin-converting enzyme ( ACE) inhibitor/angiotensin receptor blocker (ARB); coronary angiography.
Citation
AMERICAN JOURNAL OF KIDNEY DISEASES, v.60, no.4, pp.576 - 582
Journal Title
AMERICAN JOURNAL OF KIDNEY DISEASES
Volume
60
Number
4
Start Page
576
End Page
582
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16120
DOI
10.1053/j.ajkd.2012.04.017
ISSN
0272-6386
Abstract
Background: The role of the angiotensin-converting enzyme (ACE) inhibitor and angiotensin receptor blocker (ARB) in the pathophysiology of contrast-induced acute kidney injury (AKI) is controversial, and the available literature is contradictory. Study Design: A retrospective propensity score-matched study to analyze the effect of ACE-inhibitor/ARB therapy on the development of contrast-induced AKI. Setting & Participants: Using propensity score matching, 1,322 ACE-inhibitor/ARB recipients and nonrecipients were paired for analysis from 5,299 patients and fulfilled the inclusion criteria among 11,447 patients receiving coronary angiography (CAG) or percutaneous coronary intervention. Predictors: ACE-inhibitor/ARB use based on prescription and risk factors for contrast-induced AKI. Outcomes: The incidence of contrast-induced AKI defined by AKI Network (AKIN) criteria: an absolute increase in serum creatinine levels >= 0.3 mg/dL or a relative increase >= 50% from baseline values within 48 hours after exposure to the contrast medium. Measurements: Baseline serum creatinine, hemoglobin, and albumin levels; volume of contrast agents; preprocedural medication; and post-CAG serum creatinine levels. Results: An ACE inhibitor/ARB was prescribed for 64.0% of patients receiving CAG. ACE-inhibitor/ARB users showed an increased incidence of contrast-induced AKI after propensity score matching (11.4% vs 6.3%; P < 0.001). In multivariable analysis, use of ACE inhibitors/ARBs remained an independent and significant predictor of contrast-induced AKI in an unmatched cohort (OR, 1.39; 95% CI, 1.10-1.76; P = 0.06). In the matched cohort, use of ACE inhibitors/ARBs also was associated with a higher adjusted OR of contrast-induced AKI (OR, 1.43; 95% CI, 1.06-1.94; P = 0.02). Limitations: A retrospective study at a single center. Conclusions: Use of ACE inhibitors/ARBs during CAG has a possible influence to increase the incidence of contrast-induced AKI. Further randomized clinical trials are warranted to confirm the effect of ACE-inhibitor/ARB therapy on the development of contrast-induced AKI. Am J Kidney Dis. 60(4):576-582. (C) 2012 by the National Kidney Foundation, Inc.
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