Russo Elisa, Viazzi Francesca, Pontremoli Roberto, Barbagallo Carlo M, Bombelli Michele, Casiglia Edoardo, Cicero Arrigo F G, Cirillo Massimo, Cirillo Pietro, Desideri Giovambattista, D'Elia Lanfranco, Dell'Oro Raffaella, Ferri Claudio, Galletti Ferruccio, Gesualdo Loreto, Giannattasio Cristina, Iaccarino Guido, Leoncini Giovanna, Mallamaci Francesca, Maloberti Alessandro, Masi Stefano, Mengozzi Alessandro, Mazza Alberto, Muiesan Maria L, Nazzaro Pietro, Palatini Paolo, Parati Gianfranco, Rattazzi Marcello, Rivasi Giulia, Salvetti Massimo, Tikhonoff Valérie, Tocci Giuliano, Quarti Trevano Fosca A L, Ungar Andrea, Verdecchia Paolo, Virdis Agostino, Volpe Massimo, Grassi Guido, Borghi Claudio
Department of Internal Medicine, University of Genoa and IRCCS Ospdedale Policlinico San Martino, Genova, Italy.
Biomedical Department of Internal Medicine and Specialistics, University of Palermo, Palermo, Italy.
Front Cardiovasc Med. 2021 Sep 27;8:713652. doi: 10.3389/fcvm.2021.713652. eCollection 2021.
Serum uric acid predicts the onset and progression of kidney disease, and the occurrence of cardiovascular and all-cause mortality. Nevertheless, it is unclear which is the appropriate definition of hyperuricemia in presence of chronic kidney disease (CKD). Our goal was to study the independent impact of uric acid and CKD on mortality. We retrospectively investigated 21,963 patients from the URRAH study database. Hyperuricemia was defined on the basis of outcome specific cut-offs separately identified by ROC curves according to eGFR strata. The primary endpoints were cardiovascular and all-cause mortality. After a mean follow-up of 9.8 year, there were 1,582 (7.20%) cardiovascular events and 3,130 (14.25%) deaths for all causes. The incidence of cardiovascular and all-cause mortality increased in parallel with reduction of eGFR strata and with progressively higher uric acid quartiles. During 215,618 person-years of follow-up, the incidence rate for cardiovascular mortality, stratified based on eGFR (>90, between 60 and 90 and <60 ml/min) was significantly higher in patients with hyperuricemia and albuminuria (3.8, 22.1 and 19.1, respectively) as compared to those with only one risk factor or none (0.4, 2.8 and 3.1, respectively). Serum uric acid and eGFR significantly interact in determining cardiovascular and all-cause mortality. For each SUA increase of 1 mg/dl the risk for mortality increased by 10% even after adjustment for potential confounding factors included eGFR and the presence of albuminuria. hyperuricemia is a risk factor for cardiovascular and all-cause mortality additively to eGFR strata and albuminuria, in patients at cardiovascular risk.
血清尿酸可预测肾脏疾病的发生和进展,以及心血管疾病和全因死亡率的发生。然而,在慢性肾脏病(CKD)患者中,尚不清楚高尿酸血症的合适定义是什么。我们的目标是研究尿酸和CKD对死亡率的独立影响。我们对URRAH研究数据库中的21963例患者进行了回顾性调查。高尿酸血症是根据eGFR分层通过ROC曲线分别确定的特定结局临界值来定义的。主要终点是心血管疾病和全因死亡率。平均随访9.8年后,发生了1582例(7.20%)心血管事件和3130例(14.25%)全因死亡。心血管疾病和全因死亡率的发生率随着eGFR分层的降低以及尿酸四分位数的逐渐升高而平行增加。在215618人年的随访期间,与仅有一个危险因素或无危险因素的患者(分别为0.4、2.8和3.1)相比,高尿酸血症和蛋白尿患者中,基于eGFR(>90、60至90以及<60 ml/min)分层的心血管死亡率发生率显著更高(分别为3.8、22.1和19.1)。血清尿酸和eGFR在决定心血管疾病和全因死亡率方面存在显著相互作用。即使在调整了包括eGFR和蛋白尿存在等潜在混杂因素后,血清尿酸每增加1 mg/dl,死亡风险仍增加10%。在有心血管风险的患者中,高尿酸血症是心血管疾病和全因死亡率的危险因素,独立于eGFR分层和蛋白尿。