Premium
N ‐acetylcysteine for Prevention of Radiographic Contrast Material–Induced Nephropathy: Is the Intravenous Route Best?
Author(s) -
Shalansky Stephen J.,
Vu Thanh,
Pate Gordon E.,
Levin Adeera,
Humphries Karin H.,
Webb John G.
Publication year - 2005
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1592/phco.2005.25.8.1095
Subject(s) - acetylcysteine , contrast induced nephropathy , medicine , contrast (vision) , nephropathy , intravenous contrast , radiography , nuclear medicine , urology , radiology , computer science , chemistry , computed tomography , endocrinology , artificial intelligence , biochemistry , antioxidant , diabetes mellitus
Use of oral N ‐acetylcysteine for preventing radiographic contrast material–induced nephropathy (RCIN) has become widespread, despite conflicting results from clinical trials and meta‐analyses. The variability in study results may reflect differences in baseline risks in study patients, hydration regimens, choice of contrast agent, definition of RCIN, and the oral dosage formulation of N ‐acetylcysteine used. Injectable N ‐acetylcysteine recently has become available in the United States. Although oral N ‐acetylcysteine regimens are typically administered during a 48‐hour period, more rapid intravenous administration could offer an important advantage for urgent procedures such as coronary angiography. However, the three published studies in which intravenous N ‐acetylcysteine protocols were used have produced divergent results, likely because of substantially different dosage regimens. With few intravenous studies available, clinicians may look to more broadly studied oral regimens to estimate equivalent intravenous dosages. In the oral studies, however, a wide range of formulations were used, and the bioavailability of each product was uncertain. In addition, the intravenous route circumvents first‐pass metabolism, resulting in less glutathione production, perhaps compromising the antioxidant effects of N ‐acetylcysteine administration. Overall, little evidence exists that any studied N ‐acetylcysteine protocol improves clinical outcomes in terms of reducing length of hospital stay, need for dialysis, or mortality. Furthermore, N ‐acetylcysteine may directly affect serum creatinine level, which all clinical trials to date have used as a primary outcome measure. If oral or intravenous N ‐acetylcysteine is used with the intention of preventing RCIN, more‐established preventive measures should not be overlooked, including adequate hydration with isotonic saline, avoidance of potentially nephrotoxic drugs, and use of iso‐osmolar radiographic contrast media.