Background/Aims: The aim of the present study was to assess the influence of chronic angiotensin-converting enzyme (ACE) inhibitor administration on the development of contrast-induced nephropathy (CIN) in patients undergoing coronary angiography. Methods: A total of 230 patients with renal insufficiency and age ≧65 years were divided into two groups according to prior use of ACE inhibitors (ACE inhibitor group, n = 109; control group, n = 121). CIN was defined as an increase of ≧25% in creatinine over the baseline value within 48 h of angiography. Results: CIN occurred in 17 patients (15.6%) in the ACE inhibitor group and 7 patients (5.8%) in the control group (p = 0.015). Serum creatinine level increased from 1.34 ± 0.20 to 1.53 ± 0.27 mg/dl in the ACE inhibitor group and from 1.33 ± 0.18 to 1.45 ± 0.19 mg/dl in the control group (p < 0.001). Chronic ACE inhibitor administration was a risk indicator of CIN [odds ratio 3.37; 95% confidence interval 1.14–9.94; p = 0.028]. Multi-vessel coronary involvement (p = 0.001), hypoalbuminemia (p = 0.005), diabetes mellitus (p = 0.006), GFR ≤40 ml/min (p = 0.010), and congestive heart failure (p = 0.024) were other risk indicators of CIN. Conclusion: Chronic ACE inhibitor administration is a risk for developing CIN in elderly patients with renal insufficiency.

Our data support that patients with DM are at a higher risk of developing CIN, but patients with pre-DM are not at as high a risk for developing CIN as diabetes patients.

Our data support the hypothesis that patients with hyperuricemia are at risk of developing CIN.

Pre-operative vascular mapping using CDUS significantly increases the success of AVF construction and patency.

Background/Aims: Metabolic syndrome (MS) as a risk factor for contrast-induced nephropathy (CIN) has not been studied. The aim of the present study was to assess the influence of MS on the development of CIN in patients undergoing coronary angiography. Methods: This was a prospective cohort study. A total of 219 non-diabetic patients with reduced kidney function and age ≧60 years were divided into two groups (MS, n = 107 and non-MS, n = 112). CIN was defined as an increase of ≧25% in creatinine over the baseline value within 48 h of angiography. Results: CIN occurred in 14% of the MS group and 3.6% of the non-MS group (p = 0.006). Serum creatinine increased from 1.06 ± 0.17 to 1.12 ± 0.27 mg/dl in the MS group and from 1.03 ± 0.17 to 1.09 ± 0.23 mg/dl in the non-MS group (p < 0.001). MS was a risk indicator of CIN [odds ratio (OR) 4.26; 95% confidence interval (95% CI) 1.19–15.25; p = 0.026). Impaired fasting glucose (OR 4.72; 95% CI 1.53–14.56; p = 0.007), high triglyceride (OR 4.06; 95% CI 1.22–13.44; p = 0.022), and multivessel involvement (OR 3.14; 95% CI 1.07–9.82; p = 0.038) in the MS group were predictors of CIN. Conclusion: Our data support the hypothesis that patients with MS are at risk of developing CIN.