F death from CVD. Hazard ratios (HR) of CVD mortality were adjusted for gender, age, smoking- and alcoholism-related diagnoses, hypertension, hyperlipidemia, atrial fibrillation and Charlson’s comorbidity index score. Results: A case cohort (n=164,463) having gout and a control cohort (n= 3,694,377) having no gout were formed. The prevalence of gout in this study was 4.26 whereas that of gout plus CKD was 8.17 . Male to female ratio among the individuals with gout was 3.2:1. The relative risk (RR) of subsequent cardiovascular mortality between the case and control cohort was 1.71 (95 confidence interval (CI), 1.66-1.75). The presence of CKD in nondiabetic subjects with no gout (control group) has a RR of CVD mortality at 3.05 (95 CI, 2.94-3.15). The presence of gout has protective effect on subjects with CKD with a RR of 1.84 (95 CI, 1.71-1.98). As compared with individuals with no gout, the adjusted HR (aHR) for CVD mortality among the individuals with gout was 1.10 (95 CI 1.07-1.13). In a Cox model, when compared with subjects having neither gout nor CKD, the aHR in subjects with no gout but with CKD is 1.76 (95 CI, 1.70-1.82); in subjects with gout but without CKD, 1.10 (1.07-1.13); interestingly, the aHR is attenuated in subjects with concomitant gout plus CKD which is 1.38 (1.29-1.48). Conclusions: Among non-diabetic individuals aged 50 years or above who had no preceding serious CVD, those with gout were 1.1 times more likely to die from CVD as were individuals without gout. The presence of gout appears to attenuate the risk of subsequent CV mortality in subjects with CKD. Further studies should focus on finding an explanation for the protective effect of gout on CV mortality in patients with CKD.* Correspondence: [email protected]; [email protected] Equal contributors 1 Department of Biomedical Informatics, School of Computer Science, Asia University, Taichung, Taiwan 2 Department of Internal Medicine, Kuang Tien General Hospital, Taichung, Taiwan Full list of PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27689333 author information is available at the end of the article?2012 Kok et al.; licensee BioMed Central Ltd. This is an Open Access BMS-791325 supplier article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Kok et al. BMC Cardiovascular Disorders 2012, 12:108 http://www.biomedcentral.com/1471-2261/12/Page 2 ofBackground Gout is commonly seen in clinics and its prevalence has increased in recent years. It is estimated that approximately 6.1 million adults in the United States have had been diagnosed with gout [1]. Gout or hyperuricemia has long been suspected to increase the risk of cardiovascular disease [25]. A recent report from Taiwan using data from a single institute obtained via a health screening program demonstrated that the adjusted hazard ratio of cardiovascular mortality was 1.97 (95 CI 1.08, 3.59) for subjects with gout as compared with subjects with normouricemia [3]. Death from cardiovascular disease (CVD) encompassed coronary heart disease (CHD), which was manifested by myocardial infarction, angina pectoris, heart failure, and coronary death; cerebrovascular disease as manifested by stroke and/or transient ischemic attack; peripheral artery disease and aortic atherosclerosis with thoracic or abdominal aortic aneurysm. It is noted that cardiovascular events in the Asian.