Kang Eunjeong, Hwang Seung-Sik, Kim Dong Ki, Oh Kook-Hwan, Joo Kwon Wook, Kim Yon Su, Lee Hajeong
From the Department of Internal Medicine, Seoul National University Hospital; Department of Internal Medicine, Seoul National University College of Medicine; Kidney Research Institute, Seoul National University College of Medicine, Seoul; Department of Social and Preventive Medicine, Inha University School of Medicine, Incheon, Korea.
E. Kang, MD, Department of Internal Medicine, Seoul National University Hospital, and Department of Internal Medicine, Seoul National University College of Medicine; S.S. Hwang, MD, PhD, Department of Social and Preventive Medicine, Inha University School of Medicine; D.K. Kim, MD, PhD, Department of Internal Medicine, Seoul National University Hospital, and Department of Internal Medicine, Seoul National University College of Medicine, and Kidney Research Institute, Seoul National University College of Medicine; K.H. Oh, MD, PhD, Department of Internal Medicine, Seoul National University Hospital, and Kidney Research Institute, Seoul National University College of Medicine; K.W. Joo, MD, PhD, Department of Internal Medicine, Seoul National University Hospital, and Department of Internal Medicine, Seoul National University College of Medicine, and Kidney Research Institute, Seoul National University College of Medicine; Y.S. Kim, MD, PhD, Department of Internal Medicine, Seoul National University Hospital, and Department of Internal Medicine, Seoul National University College of Medicine, and Kidney Research Institute, Seoul National University College of Medicine; H. Lee, MD, Department of Internal Medicine, Seoul National University Hospital, and Department of Internal Medicine, Seoul National University College of Medicine, and Kidney Research Institute, Seoul National University College of Medicine.
J Rheumatol. 2017 Mar;44(3):380-387. doi: 10.3899/jrheum.160792. Epub 2017 Jan 15.
To explain the clinical effect of serum uric acid (SUA) levels as a risk factor for mortality, considering exclusion of kidney function.
Participants aged over 40 years who underwent health checkups were recruited. Individuals with estimated glomerular filtrations rates < 60 ml/min/1.73 m and who received laboratory study and colonoscopy on the same day were excluded.
SUA levels were higher in men than in women (5.7 ± 1.2 mg/dl for men and 4.2 ± 0.9 mg/dl for women, p < 0.001). During 12.3 ± 3.6 years of followup, 1402 deaths occurred among 27,490 participants. About 6.9% of men and 3.1% of women died. The overall mortality rate had a U-shaped association with SUA levels, a U-shaped association in men, and no association in women. There was a significant interaction of sex for the SUA-mortality association (p for interaction = 0.049); therefore, survival analysis was conducted by sex. In men, the lower SUA group had a higher mortality rate after adjustment (SUA ≤ 4.0 mg/dl, adjusted HR 1.413, 95% CI 1.158-1.724, p = 0.001) compared with the reference group (SUA 4.1-6.0 mg/dl). A higher SUA contributed to an insignificant increased mortality in men (> 8.0 mg/dl, adjusted HR 1.140, 95% CI 0.794-1.636, p = 0.479). Women failed to show any significant association between SUA and mortality.
This study provided novel evidence that SUA-mortality association differed by sex. We demonstrated that a lower SUA was an independent risk factor for all-cause mortality in men with normal kidney function.
在排除肾功能影响的情况下,解释血清尿酸(SUA)水平作为死亡风险因素的临床作用。
招募40岁以上接受健康检查的参与者。排除估算肾小球滤过率<60 ml/min/1.73 m²且在同一天接受实验室检查和结肠镜检查的个体。
男性的SUA水平高于女性(男性为5.7±1.2 mg/dl,女性为4.2±0.9 mg/dl,p<0.001)。在12.3±3.6年的随访期间,27490名参与者中有1402人死亡。男性约6.9%、女性约3.1%死亡。总体死亡率与SUA水平呈U型关联,男性呈U型关联,女性无关联。SUA与死亡率的关联存在显著的性别交互作用(交互作用p=0.049);因此,按性别进行生存分析。在男性中,与参照组(SUA 4.1 - 6.0 mg/dl)相比,调整后低SUA组死亡率更高(SUA≤4.0 mg/dl,调整后HR 1.413,95%CI 1.158 - 1.724,p = 0.001)。较高的SUA导致男性死亡率无显著增加(>8.0 mg/dl,调整后HR 1.140,95%CI 0.794 - 1.636,p = 0.479)。女性中SUA与死亡率未显示出任何显著关联。
本研究提供了新的证据,表明SUA与死亡率的关联存在性别差异。我们证明,低SUA是肾功能正常男性全因死亡率的独立风险因素。