Figure 1: Plausible synergic adverse impact of radiocontrast agents and diabetes upon the kidney, leading to contrast-induced nephropathy (CIN). Both conditions, diabetes and the administration of iodinated radiocontrast agents, lead to altered renal physiologic processes (in yellow): there is an excess formation of reactive oxygen species (ROS) and altered renal oxygenation, related to disregulated renal microcirculation and enhanced tubular transport and oxygen consumption. Evolving renal parenchymal hypoxia and enhanced ROS formation lead to tubular and vascular endothelial injury, with subsequent reduction of glomerular filtration rate (GFR), the hallmark of CIN. Conceivable interactions between these processes are outlined by arrows and discussed in depth in the text. In brief, both diabetes and contrast agents enhance ROS formation. They also hamper renal oxygenation, either directly or through increased generation of ROS. Vascular endothelial cell injury may further amplify renal hypoxia via a feed-forward loop of altered microcirculation (green arrow).