Open AccessN‐Acetylcysteine for the Prevention of Contrast‐induced Nephropathy
Author(s) -
Liu Raymond,
Nair Deepu,
Ix Joachim,
Moore Dan H.,
Bent Stephen
Publication year - 2005
Publication title -
journal of general internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.746
H-Index - 180
eISSN - 1525-1497
pISSN - 0884-8734
DOI - 10.1111/j.1525-1497.2005.30323.x
Subject(s) - medicine , acetylcysteine , nephropathy , contrast induced nephropathy , dialysis , randomized controlled trial , creatinine , renal function , acute kidney injury , incidence (geometry) , meta analysis , relative risk , confidence interval , urology , surgery , endocrinology , biochemistry , chemistry , physics , antioxidant , optics , diabetes mellitus
Objective: Contrast‐induced nephropathy is a common cause of acute renal failure in hospitalized patients. Although patients are often given N‐acetylcysteine to prevent renal injury from contrast agents, there are no clear guidelines supporting its use. We conducted a systematic review to determine whether administering N‐acetylcysteine around the time of contrast administration reduces the risk of contrast‐induced nephropathy. Design: We searched MEDLINE, EMBASE, the Cochrane Collaboration Database, bibliographies of retrieved articles, and abstracts of conference proceedings, and consulted with experts to identify relevant studies. Randomized controlled trials of N‐acetylcysteine in hospitalized patients receiving contrast were included. Studies were excluded if they did not report change in creatinine or incidence of contrast‐induced nephropathy at 48 hours. Measurements And Main Results: Nine randomized controlled trials satisfied all inclusion criteria and were included in the analysis. The difference in mean change in creatinine between the N‐acetylcysteine‐treated group and controls was −0.27 mg/dl (95% confidence interval [CI], −0.43 to −0.11). The relative risk of developing contrast‐induced nephropathy was 0.43 (95% CI, 0.24 to 0.75) in subjects randomized to N‐acetylcysteine. Significant heterogeneity existed among studies, suggesting differences in patient populations or study methodology not identified by sensitivity analyses. The incidence of dialysis was rare (0.2%). Conclusions: Our findings suggest that N‐acetylcysteine helps prevent declining renal function and contrast‐induced nephropathy. While N‐acetylcysteine is inexpensive and nontoxic, undeviating insistence for dosing at least 12 hours in advance of contrast exposure may delay diagnostic and therapeutic procedures. Future studies are needed to address the longer‐term clinical outcomes and cost‐effectiveness of this agent.