Chronic kidney disease predicts coronary plaque vulnerability

Abstract

The addition of cystatin C to creatinine in calculating the estimated glomerular filtration rate (eGFR) is known to improve the risk prediction for cardiovascular events. We sought to investigate the associations between eGFRs calculated by three Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations and coronary plaque phenotype by optical coherence tomography. We analyzed 181 nonculprit plaques from 116 coronary artery disease patients. For each patient, the eGFR was calculated using the CKD-EPIcreatinine, CKD-EPIcystatin C, and CKD-EPIcombination equations. Patients were divided into three categories according to the eGFR calculated by each equation (≥90, 60-89, and <60 ml/min/1.73 m). The prevalence of thin-cap fibroatheroma (TCFA) was correlated inversely with eGFR calculated using CKD-EPIcystatin C and CKD-EPIcombination equations, but not using the CKD-EPIcreatinine equation. The best cut-off values of eGFR calculated by these two equations for differentiating TCFA were 83 and 84 ml/min/1.73 m, respectively. Compared with the CKD-EPIcreatinine equation, patients who were reclassified upward or downward categories by the CKD-EPIcystatin C equation were associated with consistently lower [adjusted odds ratio=0.27, 95% confidence interval (CI), 0.08-0.86] and higher (adjusted odds ratio=2.41, 95% CI, 1.08-5.41) prevalence for TCFA, respectively. The net reclassification improvement with cystatin C, compared with creatinine, was 0.45 (95% CI, 0.20-0.69) for TCFA, 0.38 (95% CI, 0.09-0.67) for thrombus, and 0.21 (95% CI, 0.00-0.42) for cholesterol crystals. Results were generally similar for the CKD-EPIcombination equation. The use of cystatin C alone or in combination with creatinine, compared with creatinine alone, for GFR estimation strengthens the associations between the eGFR and prevalence of vulnerable plaque characteristics.