Pisani Antonio, Riccio Eleonora, Andreucci Michele, Faga Teresa, Ashour Michael, Di Nuzzi Antonella, Mancini Aldo, Sabbatini Massimo
Department of Nephrology, "Federico II" University of Naples, 80131 Naples, Italy.
Department of Health Sciences, "Magna Graecia" University, Catanzaro, Italy.
Biomed Res Int. 2013;2013:868321. doi: 10.1155/2013/868321. Epub 2013 Dec 29.
In vitro and in vivo studies have demonstrated enhanced hypoxia and formation of reactive oxygen species (ROS) in the kidney following the administration of iodinated contrast media, which play a relevant role in the development of contrast media-induced nephropathy. Many studies indeed support this possibility, suggesting a protective effect of ROS scavenging or reduced ROS formation with the administration of N-acetylcysteine and bicarbonate infusion, respectively. Furthermore, most risk factors, predisposing to contrast-induced nephropathy, are prone to enhanced renal parenchymal hypoxia and ROS formation. In this review, the association of renal hypoxia and ROS-mediated injury is outlined. Generated during contrast-induced renal parenchymal hypoxia, ROS may exert direct tubular and vascular endothelial injury and might further intensify renal parenchymal hypoxia by virtue of endothelial dysfunction and dysregulation of tubular transport. Preventive strategies conceivably should include inhibition of ROS generation or ROS scavenging.
体外和体内研究表明，给予碘化造影剂后，肾脏中的缺氧情况会加剧，活性氧（ROS）生成增加，这在造影剂诱导的肾病发展中起相关作用。许多研究确实支持这种可能性，分别表明给予N-乙酰半胱氨酸和输注碳酸氢盐清除ROS或减少ROS生成具有保护作用。此外，大多数易引发造影剂诱导肾病的危险因素都易于导致肾实质缺氧加剧和ROS生成增加。在本综述中，概述了肾缺氧与ROS介导损伤之间的关联。在造影剂诱导的肾实质缺氧过程中产生的ROS可能会对肾小管和血管内皮造成直接损伤，并可能由于内皮功能障碍和肾小管转运失调而进一步加剧肾实质缺氧。可以想象，预防策略应包括抑制ROS生成或清除ROS。
