Prevalence of Hyperuricemia and Gout in Mainland China from 2000 to 2014: A Systematic Review and Meta-Analysis

Li, Rui; Han, Cheng; Wu, Di; Xia, Xin; Gu, Jianqiu; Guan, Haixia; Shan, Zhongyan; Wang, Teng

doi:10.1155/2015/762820

Cited by 436 publications

(377 citation statements)

References 46 publications

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“…The prevalence is higher in developed countries perhaps as a consequence of diet, sedentary lifestyle and an increase in obesity and hypertension, reaching 21.4% among US adults (38). In China, due to rapid economic changes, the prevalence is increasing and a meta-analysis found a rate of 13.3% (39). We could not find a definite explanation for the controversial findings about the role of UA as a predictor of new-onset CKD between studies.…”

Section: Discussionmentioning

confidence: 99%

Relationship between uric acid levels and risk of chronic kidney disease in a retrospective cohort of Brazilian workers

Chini

Assis

Lugon

2017

Braz J Med Biol Res

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Uric acid (UA) levels are increased in patients with kidney dysfunction. We analyzed the association between asymptomatic hyperuricemia and new-onset chronic kidney disease (CKD). A retrospective cohort study was designed to collect data from employees of an energy generation and distribution company in the city of Rio de Janeiro, Brazil, who had undergone the company’s annual medical checkup from 2008 to 2014. People with ≤2 years of follow-up, with baseline estimated glomerular filtration rate (eGFR) <60 mL·min-1·(1.73 m2)-1 or with incomplete data were excluded. The endpoint was defined as eGFR <60 mL·min-1·(1.73 m2)-1 estimated through the chronic kidney disease epidemiology collaboration equation (CKD-EPI). The study included 1094 participants. The mean follow-up period was 5.05±1.05 years and 44 participants exhibited new-onset CKD. The prevalence of hyperuricemia was 4.2%. There was a significant inverse correlation between baseline serum levels of UA and baseline eGFR (R=-0.21, P<0.001). Female gender (OR=4.00; 95%CI=1.92-8.29, P<0.001) and age (OR=1.06; 95%CI=1.02-1.11, P=0.004) but not UA levels (OR=1.12; 95%CI=0.83-1.50; P=0.465) were associated with new-onset CKD. Diabetes mellitus and body mass index were independent factors for fast progression (OR=2.17; 95%CI=1.24-3.80, P=0.007 and OR=1.04; 95%CI=1.01-1.07; P=0.020). These results did not support UA as an independent predictor for CKD progression in the studied population.

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Section: Discussionmentioning

confidence: 99%

Relationship between uric acid levels and risk of chronic kidney disease in a retrospective cohort of Brazilian workers

Chini

Assis

Lugon

2017

Braz J Med Biol Res

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“…Significant increases in intimal areas, PCNA‐ and F4/80‐ positive cells in the carotid artery indicates that HU contributes to atherosclerosis, though no plague were found. Despite a few hundred systematic reviews, meta‐analyses, and Mendelian randomization studies exploring 136 unique health outcomes, convincing evidence of a clear causal role of urate in disease pathogenesis only exists for gout and nephrolithiasis . Urate is involved in a diverse array of biological functions, while possibly contributing to the pathogenesis of cardiovascular phenotypes, rendering it a pathogenic but not causal role .…”

Section: Discussionmentioning

confidence: 99%

Urate‐lowering therapy alleviates atherosclerosis inflammatory response factors and neointimal lesions in a mouse model of induced carotid atherosclerosis

Lü

Sun

et al. 2019

The FEBS Journal

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Hyperuricemia (HU) is a cause of gout. Clinical studies show a link between HU and cardiovascular disease. However, the role of soluble serum urate (SU) on atherosclerosis development remains elusive. We aimed to use a new HU mouse model [Uricase/Uox knockout (KO)] to further investigate the relationship between HU and atherosclerosis. A mouse model by perivascular collar placement of induced carotid atherosclerosis was established in male Uox‐ KO mice. The Uox‐ KO mice had elevated SU levels and enhanced levels of atherosclerosis inflammatory response proteins. In contrast, Uox‐ KO mice with carotid atherosclerosis showed severe neointimal changes in histology staining consistent with increases in intimal area and increases in proliferating cell nuclear antigen (PCNA)‐ and F4/80‐positive cells. Allopurinol reduced neointimal areas induced by the perivascular collar in hyperuricemic mice, accompanied by decreased expression of PCNA‐ and F4/80‐positive cells. Urate‐lowering treatment alleviated atherosclerosis inflammatory response factors and reactive oxygen species (ROS) intensities in both collar placement Uox‐ KO mice and urate‐stimulated human umbilical vein endothelial cells (HUVECs). In vitro results using HUVECs showed ROS was induced by urate and ROS induction was abrogated using antioxidants. These data demonstrate that urate per se does not trigger atherosclerosis intima lesions in male mice. Urate worsens carotid neointimal lesions induced by the perivascular collar and urate‐lowering therapy partially abrogates the effects. The current study warrants clinical studies on the possible benefits of urate‐lowering therapy in atherosclerosis patients with HU.

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“…In China, the prevalence of hyperuricemia is w13% (31), and the prevalence of tHcy concentrations $15 mmol/L is 27-30% (32,33), without the mandatory folic acid fortification of foods. In China, the estimated number of adults with hyperuricemia is 170 million, and the number of adults with tHcy concentrations $15 mmol/L is 350 million.…”

Section: Discussionmentioning

confidence: 99%

Folic acid therapy reduces serum uric acid in hypertensive patients: a substudy of the China Stroke Primary Prevention Trial (CSPPT)

Qin

et al. 2017

The American Journal of Clinical Nutrition

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Background: The effect of folic acid supplementation on uric acid (UA) concentrations is still inconclusive. Objective: We aimed to test the efficacy of folic acid therapy in reducing serum UA in hypertensive patients. Design: A total of 15,364 hypertensive patients were randomly assigned to a double-blind daily treatment with a single tablet that contained 10 mg enalapril and 0.8 mg folic acid (n = 7685) or 10 mg enalapril alone (n = 7679). The main outcome was the change in serum UA, which was defined as UA at the exit visit minus that at baseline. Secondary outcomes were as follows: 1) controlled hyperuricemia (UA concentration ,357 mmol/L after treatment) and 2) new-onset hyperuricemia in participants with normal UA concentrations (,357 mmol/L). Results: After a median of 4.4 y of treatment, the mean 6 SD UA concentration increased by 34.7 6 72.5 mmol/L in the enalaprilalone group and by 30.7 6 71.8 mmol/L in the enalapril-folic acid group, which resulted in a mean group difference of 24.0 mmol/L (95% CI: 26.5, 21.6 mmol/L; P = 0.001). Furthermore, compared with enalapril alone, enalapril-folic acid treatment showed an increase in controlled hyperuricemia (30.3% compared with 25.6%; OR: 1.31; 95% CI: 1.01, 1.70) and a decrease in new-onset hyperuricemia (15.0% compared with 16.3%; OR: 0.89; 95% CI: 0.79, 0.99). A greater beneficial effect was observed in subjects with hyperuricemia (P-interaction = 0.07) or higher concentrations of total homocysteine (tHcy) (P-interaction = 0.02) at baseline. Furthermore, there was a significant inverse relation (P , 0.001) between the reduction of tHcy and the change in UA concentrations. Conclusions: Enalapril-folic acid therapy, compared with enalapril alone, can significantly reduce the magnitude of the increase of UA concentrations in hypertensive adults. This trial was registered at clinicaltrials.gov as NCT00794885.Am J Clin Nutr 2017;105:882-9.

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Prevalence of Hyperuricemia and Gout in Mainland China from 2000 to 2014: A Systematic Review and Meta-Analysis

Cited by 436 publications

References 46 publications

Relationship between uric acid levels and risk of chronic kidney disease in a retrospective cohort of Brazilian workers

Relationship between uric acid levels and risk of chronic kidney disease in a retrospective cohort of Brazilian workers

Urate‐lowering therapy alleviates atherosclerosis inflammatory response factors and neointimal lesions in a mouse model of induced carotid atherosclerosis

Folic acid therapy reduces serum uric acid in hypertensive patients: a substudy of the China Stroke Primary Prevention Trial (CSPPT)

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