Frontiers in immunology · 2026
Serum uric acid in systemic lupus erythematosus with preserved renal function: a cross-sectional and longitudinal analysis.
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Huang Xiaolu, Chen Hongpu, Wang Yulin, Lin Fuan
Аннотация
OBJECTIVE: To evaluate the association of serum uric acid (SUA) with established lupus nephritis (LN) and to explore its prospective association with incident LN in systemic lupus erythematosus (SLE) patients presenting with preserved renal function.
METHODS: We enrolled 97 SLE patients with preserved renal function (creatinine clearance ≥ 90 mL/min), including 58 with baseline LN and 39 without LN (NLN). Baseline associations were evaluated using multivariable logistic regression, with a sensitivity model further adjusting for baseline glucocorticoid dose, mycophenolate mofetil use, and cyclophosphamide use. Model discrimination was compared by Area Under the Curve (AUC) and DeLong testing. The baseline NLN cohort was followed for 3 years, and incident LN was analyzed using a Cox model adjusted for baseline Systemic Lupus Erythematosus Disease Activity Index (SLEDAI).
RESULTS: Baseline SUA was higher in LN than in NLN patients (489.2 ± 80.8 vs. 339.8 ± 104.2 µmol/L, p < 0.001). Higher SUA remained associated with baseline LN in the main model (adjusted OR 4.20 per 1-SD increase, 95% CI 2.00-8.83, p < 0.001) and after additional adjustment for baseline treatment exposures (adjusted OR 6.32, 95% CI 1.21-32.96, p = 0.029). Adding SUA to the base clinical model increased discrimination within this dataset (AUC 0.863 to 0.929; DeLong test p = 0.001). During 3 years of follow-up, 11 NLN patients (28.2%) developed incident LN; in exploratory Cox analysis adjusted for baseline SLEDAI, higher baseline SUA was associated with a possible increased hazard of subsequent LN (adjusted HR 1.83, 95% CI 1.09-3.07, p = 0.022).
CONCLUSION: In this dataset, SUA was associated with LN risk stratification in SLE patients with preserved renal function, but this signal may also reflect broader disease activity, systemic inflammation, and treatment-related factors. The renal specificity of SUA remains uncertain.
METHODS: We enrolled 97 SLE patients with preserved renal function (creatinine clearance ≥ 90 mL/min), including 58 with baseline LN and 39 without LN (NLN). Baseline associations were evaluated using multivariable logistic regression, with a sensitivity model further adjusting for baseline glucocorticoid dose, mycophenolate mofetil use, and cyclophosphamide use. Model discrimination was compared by Area Under the Curve (AUC) and DeLong testing. The baseline NLN cohort was followed for 3 years, and incident LN was analyzed using a Cox model adjusted for baseline Systemic Lupus Erythematosus Disease Activity Index (SLEDAI).
RESULTS: Baseline SUA was higher in LN than in NLN patients (489.2 ± 80.8 vs. 339.8 ± 104.2 µmol/L, p < 0.001). Higher SUA remained associated with baseline LN in the main model (adjusted OR 4.20 per 1-SD increase, 95% CI 2.00-8.83, p < 0.001) and after additional adjustment for baseline treatment exposures (adjusted OR 6.32, 95% CI 1.21-32.96, p = 0.029). Adding SUA to the base clinical model increased discrimination within this dataset (AUC 0.863 to 0.929; DeLong test p = 0.001). During 3 years of follow-up, 11 NLN patients (28.2%) developed incident LN; in exploratory Cox analysis adjusted for baseline SLEDAI, higher baseline SUA was associated with a possible increased hazard of subsequent LN (adjusted HR 1.83, 95% CI 1.09-3.07, p = 0.022).
CONCLUSION: In this dataset, SUA was associated with LN risk stratification in SLE patients with preserved renal function, but this signal may also reflect broader disease activity, systemic inflammation, and treatment-related factors. The renal specificity of SUA remains uncertain.