Abstract
Contrast-induced nephropathy, also referred to as contrast-induced acute kidney injury (CI-AKI), is a form of AKI, with no other alternate explanation, arising from intravascular iodinated contrast media use during radiological procedures, cardiac catheterization, and percutaneous coronary intervention (PCI). The pathophysiological mechanism of CI-AKI is unknown but has been hypothesized as because of renal vasoconstriction and direct nephrotoxicity (presumably by free radicals). Although iodinated contrast media have been used for nearly a century, recognition of the association of their use with CI-AKI began in the 1960s (with the first few reported cases) and then expanded rapidly with the increase in radiological procedures, cardiac catheterization, and PCI. However, there is controversy in the medical literature about the incidence ( 30%) and prognosis of CI-AKI ( 5% requiring dialysis).1–4 The reported incidence of CI-AKI is likely exaggerated to a certain extent in the literature because of lack of appropriate controls in the studies. For example, in studies using appropriate controls, no difference in the rate of AKI has been reported in patients exposed to or not exposed to contrast media, regardless of baseline estimated glomerular filtration rate values.5 In addition, although CI-AKI has been associated with increase in short-term mortality, residual confounding in these studies makes interpretation difficult. Moreover, there is controversy over the effective preventive strategy (saline hydration, N-acetyl cysteine, sodium bicarbonate [NaHCO3], statins, or other agents) to reduce the risk of CI-AKI because of variability in the results of the randomized trials stemming from, variability in patient population studied, and variability in the treatment strategy and end point definition used. Moreover, most studies have been powered for the outcome of contrast-induced nephropathy and not for hard end points (such as death) or need for dialysis. See Article by Giacoppo et al In this …
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