Cystatin C Versus Creatinine- Based Definition of Renal Dysfunction for Predicting Poor Coronary Collateralization in Type 2 Diabetic Patients with Stable Coronary Artery DiseaseYing Shen1, Feng Hua Ding2, Feng Wu1, Zhen Sun3, Rui Yan Zhang2, Qi Zhang2, Lin Lu2,3, Zong Gui Wu1* and Wei Feng Shen2,3
- *Corresponding Author:
- Zong Gui Wu
Department of Cardiology, Chang Zheng Hospital
Second Military Medical University, 415 Feng Yang Road
Shanghai 200003, People’s Republic of China
E-mail: [email protected]
Received date: May 05, 2014; Accepted date: October 15, 2014; Published date: October 17, 2014
Citation: Shen Y, Ding FH, Wu F, Sun Z, Zhang RY, et al. (2014) Cystatin C Versus Creatinine- Based Definition of Renal Dysfunction for Predicting Poor Coronary Collateralization in Type 2 Diabetic Patients with Stable Coronary Artery Disease. J Diabetes Metab 5:453. doi: 10.4172/2155-6156.1000453
Copyright: © 2014 Shen Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objective: Renal dysfunction represents a risk factor for poor coronary collateral growth. We investigated whether Glomerular Filtration Rate (GFR) estimated with the cystatin C-based formula (GFRCYS) is superior to that with the creatinine-based abbreviated Modification of Diet in Renal Disease (GFRMDRD) and the Chronic Kidney Disease Epidemiology Collaboration (GFREPI) equations for evaluating coronary collateralization in type 2 diabetic patients with stable coronary artery disease. Methods: GFR was estimated with creatinine- and cystatin C- based equations in 302 diabetic and 127 nondiabetic patients with stable angina and angiographic total occlusion of at least one major coronary artery. The degree of collaterals supplying the distal aspect of a total occlusion from the contra-lateral vessel was graded as poor (Rentrop score of 0 or 1) or good collateralization (Rentrop score of 2 or 3). Results: In diabetic patients, GFRCYS correlated more closely with Rentrop score than GFRMDRD (Spearmen’s r=0.44 vs. Spearmen’s r=0.30, P=0.047) and GFREPI (Spearmen’s r=0.44 vs. Spearmen’s r=0.29, P=0.028), and area under the curve of GFRCYS was larger compared with that of GFRMDRD and GFREPI (0.78 vs. 0.68 and 0.66, P=0.001 and P<0.001) for predicting the presence of poor collateralization, along with a net reclassification improvement of 15.0% and 20.1% (P=0.025 and P=0.002). After adjusting for possible confounding variables, a GFR<90 mL/min/1.73m2 estimated with the cystatin C- based formula was more independently associated with poor collateralization (OR:6.21 vs. 2.86 and 2.36, P=0.042 and P=0.015). In contrast, GFRCYS, GFRMDRD, and GFREPI were similar for assessing coronary collateralization in non-diabetic patients. Conclusions: Cystatin C-based definition of renal dysfunction indicates a potential better clinical utility than creatinine-based equations for predicting poor Cystatin collaterals in diabetic atherosclerotic patients.