Contrast-Induced Acute Kidney Injury

Abstract

The development of acute kidney injury is not an uncommon complication of invasive cardiovascular procedures requiring administration of radiocontrast, and it is associated with high acute and long-term morbidity and mortality.1–3 Recognized mechanism of acute kidney injury include embolization of atheroma (cholesterol embolism), which has been shown to occur in up to 1.4% of cases in clinical studies4 and in as high as 30% of cases in pathological series,5 and a direct toxic effect of contrast media on renal tubular cells (contrast-induced acute kidney injury). In the absence of cutaneous findings associated with cholesterol embolism, and in the absence of other symptoms and signs of distal embolization, it is difficult to determine the relative contribution of cholesterol embolism to the development of acute kidney injury when compared with contrast-induced acute kidney injury. The pathophysiology of contrast-induced acute kidney injury is complex and includes a direct toxic effect on tubular cells as well as the production of reactive oxygen species.6,7 Reactive oxygen species, by acting as scavengers of NO, lead to a reduction in Po2 and to increased vascular reactivity to various vasoconstrictors including angiotensin II, thromboxane, endothelin, adenosine, and norepinephrine. During the past 2 decades, we have made substantial progress in the identification of risk factors for the development of contrast-induced acute kidney injury2,8 and in the identification of interventions that can lead to a reduction of its incidence. As of today, minimization of the total amount of contrast by modification of procedure strategies and appropriate preprocedure hydration are mainstays in the prevention of contrast-induced acute kidney injury.9–11 In addition, the use of low-osmolar and iso-osmolar contrast media has been found to be beneficial when compared with high-osmolar contrast media.12 However, substantial differences …