Response Letter
Uric Acid and Peripheral Arterial Disease
Angiology 2015, Vol. 66(7) 693 ª The Author(s) 2015 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/0003319715585235 ang.sagepub.com
Yiqiang Zhan, MD1, Ying Dong, MD, PhD2, and Jinming Yu, MD, PhD1,3
We thank Drs Sertoglu and Uyanik1 for their interest in our article2 and for providing the opportunity to discuss our findings of an association between serum uric acid (SUA) and peripheral arterial disease (PAD). Their1 suggestion that gender-specific reference values for SUA should be provided is reasonable because men and women have different distributions of SUA and diagnostic criteria for hyperuricemia. We2 categorized SUA by quartiles for men and women and found a linear trend for the association between SUA and PAD. Hence, even if the cutoff values of these quartiles are a bit different in men and women, the effects of SUA (comparing quartiles) on PAD would still show a trend. We would like to provide the results from our additional analysis, in which SUA was treated as a continuous variable because a linear trend was previously observed. This analysis provides more statistical power and efficiency for the primary objective of our study.3 We restricted our analysis in those who had estimated Glomerular Filtration Rate (eGFR) 60 mL/ min/1.73 m2. For men, a 100 mmol/L increase in SUA was associated with 9% higher odds of PAD with the corresponding odds ratio (OR) and 95% confidence interval (CI) of 1.09 (1.01-1.18) after adjusting for multiple confounders and 1.02 (0.94-1.10) after further adjusting for kidney function. For women, the corresponding values were 1.23 (1.13-1.34) and 1.15 (1.05-1.26). Thus, the main conclusion that SUA was associated with PAD and driven by kidney function remains unaltered. The reasons of sex differences in SUA and PAD remain unclear. A previous study observed a significant relationship between SUA and mean platelet volume, and this association was stronger in women than men.4 Meanwhile, platelet activation was involved in PAD pathogenesis.5 The platelet pathway might partially explain why SUA had stronger effect on PAD in women. Drs Sertoglu and Uyanik1 also suggests that patients with chronic kidney disease (CKD; estimated GFR
Uric Acid and Peripheral Arterial Disease
Angiology 2015, Vol. 66(7) 693 ª The Author(s) 2015 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/0003319715585235 ang.sagepub.com
Yiqiang Zhan, MD1, Ying Dong, MD, PhD2, and Jinming Yu, MD, PhD1,3
We thank Drs Sertoglu and Uyanik1 for their interest in our article2 and for providing the opportunity to discuss our findings of an association between serum uric acid (SUA) and peripheral arterial disease (PAD). Their1 suggestion that gender-specific reference values for SUA should be provided is reasonable because men and women have different distributions of SUA and diagnostic criteria for hyperuricemia. We2 categorized SUA by quartiles for men and women and found a linear trend for the association between SUA and PAD. Hence, even if the cutoff values of these quartiles are a bit different in men and women, the effects of SUA (comparing quartiles) on PAD would still show a trend. We would like to provide the results from our additional analysis, in which SUA was treated as a continuous variable because a linear trend was previously observed. This analysis provides more statistical power and efficiency for the primary objective of our study.3 We restricted our analysis in those who had estimated Glomerular Filtration Rate (eGFR) 60 mL/ min/1.73 m2. For men, a 100 mmol/L increase in SUA was associated with 9% higher odds of PAD with the corresponding odds ratio (OR) and 95% confidence interval (CI) of 1.09 (1.01-1.18) after adjusting for multiple confounders and 1.02 (0.94-1.10) after further adjusting for kidney function. For women, the corresponding values were 1.23 (1.13-1.34) and 1.15 (1.05-1.26). Thus, the main conclusion that SUA was associated with PAD and driven by kidney function remains unaltered. The reasons of sex differences in SUA and PAD remain unclear. A previous study observed a significant relationship between SUA and mean platelet volume, and this association was stronger in women than men.4 Meanwhile, platelet activation was involved in PAD pathogenesis.5 The platelet pathway might partially explain why SUA had stronger effect on PAD in women. Drs Sertoglu and Uyanik1 also suggests that patients with chronic kidney disease (CKD; estimated GFR
