title: The effect of N-acetylcysteine on renal function, nitric oxide, and oxidative stress after angiography.
abstract: BACKGROUND
  Renal failure induced by radiographic contrast agents is a known complication of coronary angiography, especially among patients with chronic renal failure. Recently, treatment with N-acetylcysteine (NAC) has been shown to have a protective effect but the mechanisms are unknown. We examined the hypothesis that NAC protected against contrast-induced renal impairment through effects on nitric oxide metabolism and oxidative stress.
  
  
  METHODS
  Patients with a serum creatinine concentration above 10(6) micromol/L undergoing coronary angiography were randomly assigned to receive either NAC 1 g (N= 24) or placebo (N= 29) twice daily 24 hours before and after angiography with 0.45% saline hydration in a double-blind study. Creatinine clearance was calculated and urinary nitric oxide and F2-isoprostane excretion were measured at baseline, 24 and 96 hours after angiography.
  
  
  RESULTS
  Treatment with NAC significantly improved the effect of contrast media on creatinine clearance, and maximal beneficial effect was observed 24 hours after angiography. Creatinine clearance (mL/min) was 59.5 +/- 4.4, 64.7 +/- 5.8, and 58.7 + 3.9 at baseline, 24, and 96 hours after angiography in the NAC group, respectively, and 65.2 +/- 3.2, 51.5 +/- 3.7, and 53.6 +/- 3.9 in the placebo group, respectively (P < 0.0001). NAC treatment prevented the reduction in urinary nitric oxide after angiography. The urinary nitric oxide/creatinine ratio (micromol/mg) was 0.0058 +/- 0.0004, 0.0057 +/- 0.0004, and 0.0052 +/- 0.0004 at baseline, 24, and 96 hours after angiography in NAC group, respectively, and 0.0057 +/- 0.0007, 0.0031 +/- 0.0005, and 0.0039 +/- 0.0005 in the placebo group, respectively (P= 0.013). NAC had no significant effect on urinary F2-isoprostanes.
  
  
  CONCLUSIONS
  NAC treatment has renoprotective effect in patients with mild chronic renal failure undergoing coronary angiography that may be mediated in part by an increase in nitric oxide production.
authors: Department of Medicine A, Division of Cardiology, Asaf Harofeh Medical Center, Zerifin, Israel. efratishai@barak-online.net
authors: Shai
authors: S
authors: Efrati
authors: Victor
authors: V
authors: Dishy
authors: Michael
authors: M
authors: Averbukh
authors: Alex
authors: A
authors: Blatt
authors: Ricardo
authors: R
authors: Krakover
authors: Joshua
authors: J
authors: Weisgarten
authors: Jason D
authors: JD
authors: Morrow
authors: Michael C
authors: MC
authors: Stein
authors: Ahuva
authors: A
authors: Golik
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology*; D000368:Aged; D000792:Angiography / Q000009:adverse effects*; D000975:Antioxidants / Q000494:pharmacology; D003404:Creatinine / Q000652:urine; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D007668:Kidney / Q000000981:diagnostic imaging* / Q000187:drug effects / Q000502:physiology; D007676:Kidney Failure, Chronic / Q000000981:diagnostic imaging*; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000652:urine*; D018384:Oxidative Stress / Q000187:drug effects*
chemical_list: D000975:Antioxidants; D009569:Nitric Oxide; D003404:Creatinine; D000111:Acetylcysteine