ABSTRACT
Objective:To investigate the effect of serum cystatin C level on the occurrence and its long-term prognosis of contrast agent-induced acute kidney injury(CI-AKI)after percutaneous coronary intervention(PCI)in elderly patients.Methods:A total of 848 elderly patients(≥60 years)undergoing PCI in our department between Mar 2015 and Dec 2017 were enrolled in a prospective cohort.The CI-AKI was defined as the increase of serum creatinine ≥44.2 μmol/L within 48-72 h after using iodine contrast agent or more than 25 % higher than base level within 48-72 h after PCI.A receiver operating characteristic curve was used to analyze the optimal cut-off value of Cystatin C for predicting CI-AKI after PCI.Patients were divided into 2 groups based on the optimal cut-off value of Cystatin C: the high Cystatin C group(Cystatin C ≥1.3 mg/L, n=178)and the control group(Cystatin C<1.3 mg/L, n=670). The differences in the incidence of CI-AKI after PCI and major adverse cardiac events(MACE)at 1 year follow-up were compared between the two groups.The Cox regression model was further used to analyze the predictors of the long-term prognosis after PCI.Results:Of 848 patients receiving PCI, the incidence of CI-AKI was 9.4%.The incidence of MACE at 1 year after PCI was higher in the high Cystatin C group than in the control group(15.7% vs.9.3%, χ2=6.524, P=0.011). Cox regression analysis confirmed that the high baseline level of Cystatin C was the most independent predictive factor for MACE at 1 year of follow-up( HR=16.244, P<0.001). Conclusions:The high baseline level of Cystatin C(≥1.3 mg/L)is an independent risk factor for CI-AKI and is also the most important predictor for the occurrence of long-term MACE in elderly patients undergoing PCI.
ABSTRACT
Adiponectin is an adipocyte-specific adipocytokine that possesses anti-atherogenic and anti-diabetic properties. It has been shown to have a beneficial effect on the cardiovascular system, but it remains to be elucidated whether adiponectin has a therapeutic effect on vascular damage induced by the potential vasoactive substance angiotensin II (Ang II). In this study, the effects of adiponectin on Ang II-induced vascular endothelial damage were investigated. In cultured human umbilical vein endothelium cells, Ang II stimulation increased generation of ROS and 4-hydroxy-2-nonenal, both of which were clearly restored by administration of adiponectin. In addition, administration of adiponectin was found to increase cell viability and prevent apoptosis. Our results also demonstrate that the protective effects of adiponectin against Ang II-induced vascular endothelial damage are dependent on the binding of adiponectin to its cell surface receptor 1. Importantly, we found that adiponectin treatment modulates the apoptotic pathway by reducing the expression of LOX-1, up-regulating both cIAP-1 and the ratio of Bcl-2/Bax. Finally, our data displayed that the protective effects of adiponectin against Ang II cytotoxicity depend on AMPK activation mediated by the endosomal adaptor protein, adaptor protein with phosphotyrosine binding, pleckstrin homology domains, and leucine zipper motif.
