Reply to: uric acid and contrast-induced nephropathy: diagnostic marker, therapeutic target, or innocent bystander?

Abstract

We thank Canpolat and colleagues for their interest in our paper. Firstly, they mention that the SYNTAX score was not calculated in our study. This valuable comment warrants consideration in future studies. Secondly, the authors requested a comment on whether serum uric acid (SUA) level in the development of contrast-induced acute kidney injury (CI-AKI) was a diagnostic marker or an innocent bystander. A recent meta-analysis conducted by our group concluded that an elevated SUA level is a risk factor for the development of CI-AKI. In addition, 2 clinical trials, discussed in this meta-analysis, suggested that lowering SUA levels with allopurinol may prevent CI-AKI. We therefore speculate that SUA is an independent risk factor for CI-AKI. Postulated mechanisms include that SUA may increase oxidative stress as well as activate cytokines and inflammation, which leads to endothelial dysfunction, reduced renal blood flow, increased renal vascular resistance, and may cause crystallization and tubular luminal obstruction. Therefore, SUA may be an independent player in the pathogenesis of CI-AKI. Thirdly, the authors enquired regarding the subtypes of statin therapy used. Unfortunately, details with respect to dose and type of statins were unavailable in the records. Consequently, we were unable to carry out a subanalysis of statin therapy, and this is a limitation of our study. In our study, we included well-known established risk factors for the development of contrast-induced nephropathy (CIN) in multivariate analysis to show independent associations between CIN and SUA. In conclusion, the findings of our study, and previous studies, may help understand the pathophysiology of CI-AKI and identify novel strategies for preventing CI-AKI.