Dyslipidemia is frequently observed in patients with systemic lupus erythematosus (SLE) accompanied by hypocomplementemia, suggesting a link between immune dysregulation and lipid metabolism. The complement system, a critical component of innate immunity, plays a pivotal role in immune complex clearance and inflammatory regulation. Dysregulation of complement activity has been implicated in the pathogenesis of SLE, contributing to chronic inflammation and end-organ damage.Moreover, dyslipidemia in SLE is not merely a metabolic comorbidity but may also contribute to accelerated atherosclerosis and cardiovascular events, which represent leading causes of morbidity and mortality in this population.This study aims to evaluate the association between complement components and lipid profiles, and investigate their impact on organ involvement in SLE patients.

A total of 935 patients with SLE were enrolled and stratified by baseline lipid profiles. Logistic regression, stratified analyses, and Receiver Operating Characteristic (ROC) curve analyses were employed to assess the predictive value of complement levels and other clinical factors for dyslipidemia and organ damage.

Among the 935 patients, 527 (56.4%) were diagnosed with dyslipidemia. The dyslipidemia group exhibited significantly higher erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels, alongside lower complement 3 (C3) levels compared to the non-dyslipidemia group. Decreased C3 levels were independently associated with an increased risk of dyslipidemia (OR = 0.29, 95% CI: 0.18–0.47, P < 0.0001) and renal involvement (OR = 0.21, 95% CI: 0.12–0.37, P < 0.0001). This association was further pronounced in patients with C3 ≤ 0.7 g/L (OR = 0.08, 95% CI: 0.01–0.48, P = 0.0061). A predictive model for dyslipidemia was developed: using a C3 threshold of ≤ 0.68 g/L and an ESR threshold of ≥ 33.65 mm/h, the model achieved a sensitivity of 64.1%, a specificity of 74.7%, and an AUC of 0.71.

Reduced C3 levels serve as a significant independent risk factor for both dyslipidemia and renal involvement in SLE. Furthermore, the combined assessment of C3 and ESR enhances the clinical identification of dyslipidemia risk.