Abstract

IntroductionTo explore whether dyslipidemia, hyperglycemia or hypertension has mediating effect on the association between serum uric acid (SUA) and the development of chronic kidney disease (CKD).MethodsWe conducted a mediation analysis to explore the potential mediating effects of systolic blood pressure (SBP), diastolic blood pressure (DBP), blood glucose, triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) on the association between SUA and estimated glomerular filtration rate (eGFR). The data were obtained from China Health and Retirement Longitudinal Study (CHARLS), covering 5,762 individuals.ResultsSUA had a negative dose-response total effect on eGFR (β -3.11, 95% CI -3.40 to -2.82, P-value<0.001). The linear regression between SUA and seven potential mediators indicated that blood glucose (β 0.80, 95% CI 0.18 to 1.42, P-value=0.012), TG (β 10.01, 95% CI 8.22 to 11.79, P-value<0.001), TC (β 2.64, 95% CI 1.83 to 3.45, P-value<0.001), HDL-C (β -0.27, 95% CI -0.52 to -0.02, P-value=0.034) and LDL-C (β 1.15, 95% CI 0.49 to 1.80, P-value=0.001) all had significant dose-response association with SUA, but SBP and DBP showed no significant association with SUA. In terms of the association between potential mediators and eGFR, only TG (β 0.003, 95% CI -0.001 to 0.01, P-value=0.117) and HDL-C (β 0.01, 95% CI -0.02 to 0.04, P-value=0.444) did not have significant linear association with eGFR. The linear regression showed that SUA was directly associated with eGFR (P-value<0.001).ConclusionsThis study supported that the association between SUA and the risk of CKD was not mediated by hypertension, hyperglycemia or dyslipidemia.

Highlights

  • To explore whether dyslipidemia, hyperglycemia or hypertension has mediating effect on the association between serum uric acid (SUA) and the development of chronic kidney disease (CKD)

  • The linear regression between SUA and seven potential mediators indicated that blood glucose (b 0.80, 95% CI 0.18 to 1.42, P-value=0.012), TG (b 10.01, 95% CI 8.22 to 11.79, P-value

  • This study supported that the association between SUA and the risk of CKD was not mediated by hypertension, hyperglycemia or dyslipidemia

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Summary

Introduction

Hyperglycemia or hypertension has mediating effect on the association between serum uric acid (SUA) and the development of chronic kidney disease (CKD). Serum uric acid (SUA), the end product of purine metabolism in humans [5], has gradually been considered as a risk factor of CKD [6,7,8,9,10,11]. Existing evidence has suggested that elevated SUA concentration may play a role in the development of CKD [7, 8], which may be mediated by cardiometabolic factors. Limited studies have examined the mediating effect of such cardiometabolic factors on the association between SUA and CKD; whether dyslipidemia, hyperglycemia or hypertension has mediating effect on the association between SUA and the development of CKD remains unclear

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