Background and aims Decreased nitric oxide (NO) bioavailability and increased oxidative stress may be involved in the pathogenesis of contrast-induced acute kidney injury (CI-AKI). The relationship between asymmetric dimethylarginine (ADMA), an endogenous NO synthase inhibitor, and CI-AKI is unknown. Methods We measured plasma ADMA levels in 664 consecutive subjects undergoing cardiac catheterization. Mehran score for predicting the risk of CI-AKI was calculated. Results After cardiac catheterization, 78 (11.7%) patients experienced CI-AKI (defined as increase of serum creatinine levels of ≥0.3 mg/dl or a 25% increase from baseline value at 48 h after the procedure). The plasma ADMA levels of patients with CI-AKI were significantly higher than those of patients without CI-AKI (0.50 ± 0.09 μmol/l versus 0.46 ± 0.10 μmol/l, p < 0.001). The c-statistics of plasma ADMA level and Mehran score for the occurrence of CI-AKI were 0.639 (95% CI: 0.601–0.676, p < 0.001) and 0.615 (95% CI: 0.577–0.652, p = 0.001), respectively. By using a cutpoint of plasma ADMA level of 0.42 μmol/l, the analysis would yield 85.9% sensitivity, 37.0% specificity. Adding the plasma ADMA level to the Mehran score system marginally increases the c-statistic from 0.615 to 0.643 (p = 0.03). Furthermore, in patients developing CI-AKI, those with plasma ADMA levels >0.42 μmol/l (14 events in 52 patients) tended to have a higher 1-year major adverse event rate than those with plasma ADMA level ≤0.42 μmol/l (2 events in 26 patients) (p = 0.055). Conclusions In patients undergoing cardiac catheterization, ADMA might be a novel risk factor of CI-AKI.
|Number of pages||6|
|State||Published - 1 Nov 2016|
- Asymmetric dimethylarginine
- Contrast medium
- Contrast-induced acute kidney injury
- Nitric oxide