Dose-response analysis of serum uric acid levels and the risk of developing chronic kidney disease in patients with gout

 

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Dose-response analysis of serum uric acid levels and the risk of developing chronic kidney disease in patients with gout

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Serong
Wang
Serong Wang 2095298168@qq.com Guiyang Ankylosing Hospital Guiyang Ankylosing Hospital Chengdu China *
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Globally, the prevalence of hyperuricemia (HUA) has exceeded 20% and is shifting toward younger age groups. Chronic kidney disease (CKD) is a common complication of gout, with approximately 24% of gout patients progressing to stage Ⅲ or higher CKD. However, the dose-response relationship between serum uric acid (SUA) levels and CKD development in gout patients remains unexplored. This study, focusing on gout patients in Southwest China, aimed to investigate the relationship and dose-response relationship between SUA levels and CKD risk, providing a scientific basis for CKD prevention and management.

We collected clinical data from 502 gout patients who visited our hospital between February 2023 and February 2024. Gout diagnosis was based on the criteria established by the 2015 American College of Rheumatology (ACR) guidelines. The estimated glomerular filtration rate (eGFR) was calculated based on creatinine levels using the CKD Epidemiology Collaboration 2021 (CKD-EPI) equation, with CKD defined as eGFR < 60 ml/min/1.73 m². Patients were divided into two groups based on eGFR: the CKD group (eGFR < 60 ml/min/1.73 m²) and the non-CKD group (eGFR 60 ml/min/1.73 m²). Multivariate logistic regression was used to assess the association with CKD. A three-node restricted cubic spline (RCS) was employed to model the dose-response relationship between SUA levels and the development of CKD, based on model 2. P-values < 0.05 were considered statistically significant.

The mean SUA was higher in CKD patients (629.15 μmol/l) compared to non-CKD patients (581.2 μmol/l), (P = 0.006) (Table 1). No significant association was found between CKD and gouty arthritis (χ = 2.332, P = 0.267). However, the presence of CKD was significantly linked to the development of gouty stones (χ = 6.028, P = 0.022). Additionally, three models were developed to adjust for confounders and further examine the relationship between SUA and CKD (Table 2). The results indicated a strong positive correlation between SUA and CKD. In the unadjusted model, the odds ratio (OR) was 1.002, with a 95% confidence interval (CI) of 1.000 to 1.004 (P = 0.023). This positive association remained statistically significant after adjusting for all confounders in Model 3 (P = 0.034). Using Model 2, the dose-response relationship between CKD and HUA was further explored through RCS analysis. The continuous change in SUA was plotted on the horizontal axis, while the risk of CKD occurrence was plotted on the vertical axis. The results revealed a significant association between SUA levels and CKD incidence risk (P = 0.035). However, the non-linear relationship was not significant, suggesting a more linear association. This implies that the risk of CKD may exhibit a regular upward or downward trend as SUA levels change, rather than a complex curvilinear relationship (Figure 1).

In gout patients, serum uric acid (SUA) is a significant risk factor for the development of CKD, with the risk of CKD exhibiting a consistent upward or downward trend as SUA levels change. This study offers valuable scientific evidence for the prevention and management of CKD in gout patients, emphasizing that close monitoring of SUA levels and timely intervention could reduce CKD risk and improve clinical outcomes.

 

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