Renalguard system: A dedicated device to prevent contrast-induced acute kidney injury

摘要

Contrast-induced acute kidney injury (CI-AK1) is the third most common cause of hospital-acquired AKI, accounting for more than 10% of cases. Approximately half of these cases occur in patients undergoing iodinated contrast media (CM) exposure due to cardiac catheterization and angiography, and about one third follow computed tomography. Hemodynamic changes of renal blood flow, which lead to hypoxia of the renal medulla, and direct toxic effects of CM on renal cells are thought to contribute to the pathogenesis of CI-AKI. CM induce renal cell apoptosis through the activation of the intrinsic pathway. The steps leading to the final activation of the intrinsic (or mitochondrial) apoptotic pathway are: 1) the increase in membrane reactive oxygen species (ROS) production, 2) the activation of the stress kinases JNK1/2 and p38; and 3) the increase of expression levels of the Bcl2-family pro-apoptotic proteins BAX, BAK and BAD, and 4) the final increases in caspase-9 and caspase-3 activities. Both ROS activation and the eventual apoptotic damage are dose- and time-dependent. This underscores 2 important aspects of contrast-induced kidney damage, with important significance in the clinical setting: 1) the need of a quick elimination of the CM from the kidney, and 2) the volume of CM media should be minimized.