Abstract 893: Contrast Medium-Induced Renal Damage is Tightly Associated with Endothelial Injury in Patients
Background: Contrast-induced nephropathy (CIN) remains a common complication of radiographic procedures. We hypothesized that endothelial dysfunction is the main cause of CIN. To clarify whether contrast medium-induced renal damage is associated with endothelial injury, we measured microparticles derived from endothelial cells as markers of endothelial injury. Circulating microparticles are shed from cell surface respond to cell activation and apoptotic stimuli, reflecting the condition of damaged cells.
Methods: Renal function of 35 adult patients was analyzed before and after the use of contrast medium for coronary angiography. Parameters for renal function and urinary 15-isoprostane F2t, a specific marker of oxidative stress were measured before and after radiocontrast administration. Flow cytometry was used to count circulating CD34+ microparticles, which is regarded as one of markers for endothelial damage.
Results: The decrease of estimated glomerular filtration rate positively correlated with the amount of contrast medium (r=0.427; P=0.013). Urinary N-acetyl-beta-D-glucosaminidase, a marker of renal tubular injury, was increased after angiography (from 7.6+/− 6.8 to 9.1 +/− 6.0 U/g-CRE, P=0.011). Furthermore, urinary 15-isoprostane F2t positively correlated with the volume of contrast medium (r=0.421; P=0.012). CD34+ microparticle was significantly increased after angiography (1.3-fold increased from basal level, P=0.0017). The increase of CD34+ microparticle was associated with the insult of contrast medium, but not of the amount.
Conclusion: Radiocontrast impaired renal function in accordant with the increase of oxidative stress. The release of CD34+ microparticle was also increased by use of radiocontrast. These data suggest that CIN is tightly associated with endothelial injury mediated by radiocontrast-induced oxidative stress.