Borghi Claudio, Rosei Enrico Agabiti, Bardin Thomas, Dawson Jesse, Dominiczak Anna, Kielstein Jan T, Manolis Athanasios J, Perez-Ruiz Fernando, Mancia Giuseppe
aDepartment of Medical and Surgical Sciences, University of Bologna, Bologna, Italy bDepartment of Clinical and Experimental Sciences, University of Brescia, Department of Medicine, Spedali Civili, Brescia, Italy cAssistance Publique Hôpitaux de Paris, Hôpital Lariboisière dUniversité Paris Diderot, Sorbonne Paris Cité eINSERM, UMR 1132, Paris, France fInstitute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK gDepartment of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany hCardiology Department, Asklepeion Hospital, Athens, Greece iRheumatology Division, Hospital Universitario Cruces and Biocruces Health Research Institute, Vizcaya, Spain jUniversità Milano-Bicocca, IRCCS Istituto Auxologico Italiano, Milan, Italy.
J Hypertens. 2015 Sep;33(9):1729-41; discussion 1741. doi: 10.1097/HJH.0000000000000701.
Substantial evidence suggests that chronic hyperuricemia is an independent risk factor for hypertension, metabolic syndrome, chronic kidney disease (CKD) and cardiovascular diseases. This highlights the need for greater attention to serum uric acid levels when profiling patients, and suggests that the threshold above which uricemia is considered abnormal is 6 mg/dl, in light of the available evidence. Another important question is whether lowering serum uric acid can improve cardiovascular and renal outcomes, and what therapeutic mechanism of action could provide more clinical benefits to patients; the available literature shows a trend toward improvement associated with administration of urate-lowering drugs, in particular for the xanthine oxidase inhibitors. The demonstrated efficacy of urate-lowering therapy on outcomes other than gout flares leads to the consideration that treatment may be beneficial even in the absence of overt gout when hyperuricemia accompanies other clinical conditions, such as urate deposition, advanced CKD or cardiovascular risk factors.
大量证据表明，慢性高尿酸血症是高血压、代谢综合征、慢性肾脏病（CKD）和心血管疾病的独立危险因素。这凸显了在对患者进行病情分析时，需要更加关注血清尿酸水平，并且根据现有证据表明，血尿酸水平被认为异常的阈值是6毫克/分升。另一个重要问题是，降低血清尿酸是否能改善心血管和肾脏结局，以及何种治疗作用机制能为患者带来更多临床益处；现有文献表明，使用降尿酸药物有改善病情的趋势，尤其是黄嘌呤氧化酶抑制剂。降尿酸治疗对痛风发作以外的结局所显示出的疗效，让人认为即使在没有明显痛风但高尿酸血症伴有其他临床情况（如尿酸盐沉积、晚期CKD或心血管危险因素）时，治疗可能也是有益的。
