Reduction of circulating endothelial progenitor cell level is associated with contrast-induced nephropathy in patients undergoing percutaneous coronary and peripheral interventions

PLoS One. 2014 Mar 19;9(3):e89942. doi: 10.1371/journal.pone.0089942. eCollection 2014.

Abstract

Objectives: Reduced 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 results: A 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.

Conclusions: Decreased 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Angioplasty / adverse effects*
  • Antigens, CD / metabolism
  • Biomarkers / analysis
  • Cell Count
  • Contrast Media / adverse effects*
  • Creatinine / blood
  • Endothelial Progenitor Cells / pathology*
  • Female
  • Humans
  • Male
  • Middle Aged
  • Nephrosis / chemically induced
  • Nephrosis / diagnosis*
  • Nephrosis / mortality
  • Nephrosis / pathology
  • Percutaneous Coronary Intervention / adverse effects*
  • Survival Analysis

Substances

  • Antigens, CD
  • Biomarkers
  • Contrast Media
  • Creatinine

Grants and funding

This study was supported in part by research grants from the NSC 97-2314-B-075-039, NSC 98-2314-B-075-035, and UST-UCSD International Center of Excellence in Advanced Bio-engineering NSC-99-2911-I-009-101 from the National Science Council; VGH-V98B1-003 and VGH-V100E2-002 from Taipei Veterans General Hospital, and also a grant from the Ministry of Education “Aim for the Top University” Plan. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.