title: Prediction of chronic renal insufficiency after coronary angiography by an early increase in oxidative stress and decrease in glomerular filtration rate.
abstract: BACKGROUND
  Oxidative stress caused by contrast medium is thought to be one of the main mechanisms of contrast-induced acute kidney injury. A prospective study was conducted to evaluate the relationship between oxidative stress caused by contrast agent administration and long-term renal function.
  
  
  RESULTS
  Thirty-six consecutive patients who underwent coronary angiography were enrolled. Urinary F2-isoprostane, a marker of oxidative stress, was measured at baseline and 24h after angiography, and serum creatinine was measured at baseline, 24h and 1 year after the procedure. The change in estimated glomerular filtration rate (eGFR) at 1 year after angiography correlated significantly with the change in eGFR at 24h after angiography (r=0.729, P<0.001). We also found a significant correlation between the increase in urinary F2-isoprostane at 24h and the decrease in eGFR at 1 year (r=0.439, P=0.022). In multivariate analysis, the decrease in eGFR at 1 year after coronary angiography correlated with the increase in F2-isoprostane at 24h after angiography as well as the decrease in eGFR at 24h after angiography (P=0.039 and P<0.001, respectively).
  
  
  CONCLUSIONS
  Contrast-induced nephrotoxicity might be transient; however, an early decrease in eGFR and increase in oxidative stress are associated with chronic renal insufficiency. Careful long-term follow-up and adequate medical intervention are necessary for these patients.
authors.affiliation: Cardiovascular Division, Institute of Clinical Medicine, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
authors.forename: Kazuko
authors.initials: K
authors.lastname: Tajiri
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Maruyama
authors.forename: Akira
authors.initials: A
authors.lastname: Sato
authors.forename: Nobutake
authors.initials: N
authors.lastname: Shimojo
authors.forename: Takumi
authors.initials: T
authors.lastname: Saito
authors.forename: Masae
authors.initials: M
authors.lastname: Endo
authors.forename: Hideaki
authors.initials: H
authors.lastname: Aihara
authors.forename: Satoru
authors.initials: S
authors.lastname: Kawano
authors.forename: Shigeyuki
authors.initials: S
authors.lastname: Watanabe
authors.forename: Satoshi
authors.initials: S
authors.lastname: Sakai
authors.forename: Kazutaka
authors.initials: K
authors.lastname: Aonuma
mesh_terms: D000118:Acetylglucosaminidase / Q000097:blood; D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000150:complications / Q000378:metabolism; D000368:Aged; D015415:Biomarkers; D003287:Contrast Media / Q000009:adverse effects*; D017023:Coronary Angiography; D003404:Creatinine / Q000097:blood; D003920:Diabetes Mellitus / Q000453:epidemiology; D050171:Dyslipidemias / Q000453:epidemiology; D028441:F2-Isoprostanes / Q000652:urine*; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D006973:Hypertension / Q000453:epidemiology; D007479:Iopamidol / Q000009:adverse effects / Q000031:analogs & derivatives*; D007676:Kidney Failure, Chronic / Q000453:epidemiology* / Q000209:etiology / Q000378:metabolism; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D003287:Contrast Media; D028441:F2-Isoprostanes; C057937:iomeprol; D003404:Creatinine; D000118:Acetylglucosaminidase; D007479:Iopamidol