Eunjeong Kang1,2, Seung-Sik Hwang1,2, Dong Ki Kim1,2, Kook-Hwan Oh1,2, Kwon Wook Joo1,2, Yon Su Kim1,2, Hajeong Lee3,4. 1. 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. 2. 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. 3. 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. mdhjlee@gmail.com. 4. 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. mdhjlee@gmail.com.
Abstract
OBJECTIVE: To explain the clinical effect of serum uric acid (SUA) levels as a risk factor for mortality, considering exclusion of kidney function. METHODS: Participants aged over 40 years who underwent health checkups were recruited. Individuals with estimated glomerular filtrations rates < 60 ml/min/1.73 m2 and who received laboratory study and colonoscopy on the same day were excluded. RESULTS: 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. CONCLUSION: 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.
OBJECTIVE: To explain the clinical effect of serum uric acid (SUA) levels as a risk factor for mortality, considering exclusion of kidney function. METHODS:Participants aged over 40 years who underwent health checkups were recruited. Individuals with estimated glomerular filtrations rates < 60 ml/min/1.73 m2 and who received laboratory study and colonoscopy on the same day were excluded. RESULTS: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. CONCLUSION: 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.
Authors: Eunjeong Kang; Jina Park; Hyo Jeong Kim; Sehoon Park; Minsu Park; Yaerim Kim; Kwangsoo Kim; Sang Min Park; Dong-Wan Chae; Ho Jun Chin; Jung Pyo Lee; Sik Lee; Soo Wan Kim; Jang-Hee Cho; Miyeun Han; Yong Chul Kim; Yon Su Kim; Insun Choi; Hajeong Lee Journal: Kidney Res Clin Pract Date: 2021-10-12