2005
DOI: 10.1093/ndt/gfh868
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Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art

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Cited by 146 publications
(155 citation statements)
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“…Interestingly, in animal studies, both intravenous contrast dye 37,38 and highdose vancomycin 15,16 have been demonstrated to promote free radical formation within renal tissue, which is hypothesized to cause tubular damage primarily through vascular endothelial dysfunction, vasoconstriction, and subsequent reperfusion injury. N-acetylcysteine is frequently administered to patients about to receive intravenous contrast dye (although its benefit remains controversial 37,39 ); N-acetylcysteine has also been shown in an animal model to attenuate vancomycin-induced renal injury. 40 Receipt of concomitant aminoglycosides was not significantly associated with nephrotoxicity, in contrast with previous studies.…”
Section: Discussionmentioning
confidence: 99%
“…Interestingly, in animal studies, both intravenous contrast dye 37,38 and highdose vancomycin 15,16 have been demonstrated to promote free radical formation within renal tissue, which is hypothesized to cause tubular damage primarily through vascular endothelial dysfunction, vasoconstriction, and subsequent reperfusion injury. N-acetylcysteine is frequently administered to patients about to receive intravenous contrast dye (although its benefit remains controversial 37,39 ); N-acetylcysteine has also been shown in an animal model to attenuate vancomycin-induced renal injury. 40 Receipt of concomitant aminoglycosides was not significantly associated with nephrotoxicity, in contrast with previous studies.…”
Section: Discussionmentioning
confidence: 99%
“…Probably the most frequent under-estimated factor which contributes to acute renal dysfunction after cardiac cathetherism is cholesterol embolism, often asymptomatic, but present in up to 50% of cases [13]. [14,15]. Briefly, there is a determinant contribution of hemodynamic alterations, endothelial dysfunction, vasoactive mediators, rheologic factors, free oxygen radicals release, immunological mechanisms, direct tubular toxicity and other mechanisms.…”
Section: Risk Factors For Radiocontrast-induced Nephropathymentioning
confidence: 99%
“…For this reason, taking the appropriate prophylactic regimens is important in reducing CIN. [1] It had been postulated that antioxidant N-acetylcysteine (NAC) might scavenge oxygen free radicals and thus attenuate the cytotoxic effects of contrast media. [2,3] Tepel et al evaluated the effects of NAC (600 mg orally twice daily), at first time, in 83 patients undergoing computed tomography.…”
mentioning
confidence: 99%
“…While many trials have shown benefit, more recent investigation has found conflicting results of the effect of NAC on prevention of CIN. [1][2][3] In most of the NAC studies, a rise in serum creatinine by ≥ 0.5 mg/dL or ≥ 25% above baseline at 48-72 h after contrast exposure was used as the primary outcome. Due to dietary creatinine intake, tubularly secretion of creatinine, and variations in the patient's muscle mass, the use of serum creatinine may inaccurately estimate the glomerular filtration rate (GFR).…”
mentioning
confidence: 99%
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