Abstract Lupus nephritis (LN), a significant complication of systemic lupus erythematosus, remains a major cause of morbidity and mortality due to its impact on renal function. Recent attention has been directed toward uric acid (UA) as a potential contributor to LN pathogenesis. This review consolidates existing literature to explore UA’s dual role as both a marker and mediator in LN. Elevated serum UA levels are associated with oxidative stress, endothelial dysfunction, and inflammation, all of which exacerbate renal injury and correlate with disease severity. Mechanistic insights reveal UA’s activation of pro-inflammatory pathways, including the NLRP3 inflammasome, contributing to glomerular damage and proteinuria. Observational studies further highlight UA’s predictive value in chronic kidney disease progression and renal fibrosis. Despite promising findings, the integration of UA as a biomarker and therapeutic target in LN is limited by heterogeneity in study methodologies and demographic variability. This synthesis underscores the potential of UA-lowering therapies while calling for standardized measurement protocols, demographic-specific analyses, and robust interventional trials to optimize LN management.
Mazen Abdallah Al Zo’ubi (Tue,) studied this question.