Reduction of Circulating Endothelial Progenitor Cell Level Is Associated with Contrast-Induced Nephropathy in Patients Undergoing Percutaneous Coronary and Peripheral Interventions

Chia-Hung Chiang,Chin-Chou Huang,Chun-Chih Chiu,Chien-Yi Hsu,Jaw-Wen Chen,Shing-Jong Lin,Po-Hsun Huang,Hsin-Bang Leu,Zoran Ivanovic

doi:10.1371/journal.pone.0089942

Abstract

ObjectivesReduced number and impaired function of circulating endothelial progenitor cells (EPCs) in patients with chronic kidney disease have been reported. However, there is little data about the association between circulating EPC levels and risk of contrast-induced nephropathy (CIN). The aim of this study was to investigate the relationship between circulating EPCs and CIN in patients after angiography.Methods and ResultsA total of 77 consecutive patients undergoing elective percutaneous coronary intervention (PCI) and percutaneous transluminal angioplasty (PTA) were enrolled. Flow cytometry with quantification of EPC markers (defined as CD34+, CD34+KDR+, and CD34+KDR+CD133+) in peripheral blood samples was used to assess EPC number before the procedure. CIN was defined as an absolute increase ≧0.5 mg/dl or a relative increase ≧25% in the serum creatinine level at 48 hours after the procedure. Eighteen (24%) of the study subjects developed CIN. Circulating EPC levels were significantly lower in patients who developed CIN than in those without CIN (CD34+KDR+, 4.11±2.59 vs. 9.25±6.30 cells/105 events, P<0.001). The incidence of CIN was significantly greater in patients in the lowest EPC tertile (CD34+KDR+; from lowest to highest, 52%, 15%, and 4%, P<0.001). Using univariate logistic regression, circulating EPC number (CD34+KDR+) was a significant negative predictor for development of CIN (odds ratio 0.69, 95% CI 0.54–0.87, P = 0.002). Over a two-year follow-up, patients with CIN had a higher incidence of major adverse cardiovascular events including myocardial infarction, stroke, revascularization of treated vessels, and death (66.7% vs. 25.4%, P = 0.004) than did patients without CIN.ConclusionsDecreased EPC level is associated with a greater risk of CIN, which may explain part of the pathophysiology of CIN and the poor prognosis in CIN patients.

Highlights

Contrast-induced nephropathy (CIN) remains a serious clinical problem in the use of iodinated contrast media [1,2]
Decreased endothelial progenitor cells (EPCs) level is associated with a greater risk of contrast-induced nephropathy (CIN), which may explain part of the pathophysiology of CIN and the poor prognosis in CIN patients
Patients, who were older than 18 years of age, with normal to subnormal GFR, and scheduled for elective cardiovascular procedures including percutaneous coronary intervention (PCI) and percutaneous transluminal angioplasty (PTA), were eligible for this study

Summary

Introduction

Contrast-induced nephropathy (CIN) remains a serious clinical problem in the use of iodinated contrast media [1,2]. Increasing use of contrast media in interventional procedures has led to a parallel increase in the incidence of CIN, despite the use of newer and less nephrotoxic contrast agents in high-risk patients in recent years. Its development has been associated with increased in-hospital and long-term morbidity and mortality, prolonged hospitalization, and long-term renal impairment [4]. Proposed pathophysiologic mechanisms through which contrast administration may potentiate renal injury include oxidative stress, free radical damage, and endothelial dysfunction [5,6]. The actual pathogenesis of CIN and the pathophysiologic mechanisms underlying the evolution from CIN to atherosclerosis and cardiovascular events remain to be determined

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