Inflammatory Mediators in Kidney Disease: A Focus on IL-6in SLE-Associated CKD.
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INTRODUCTION: Systemic lupus erythematosus (SLE) is an autoimmune condition that can lead to severe renal impairment, including chronic kidney disease (CKD) or end-stage kidney disease (ESKD). This study aimed to evaluate the serum levels of key pro-inflammatory cytokines which are well-known to mediate tissue injury and fibrosis in the context of kidney diseases-interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α), and IL-12-in CKD and ESKD patients with and without SLE, as well as in healthy controls, to explore their role in disease progression. METHODS: This cross-sectional study was conducted over a 15-month period in three governmental medical centers of Golestan Province, Iran (Sayyad Shirazi Hospital, 5th Azar hospital, and Al-Jalil hospital). A total of 118 individuals (age 18-65 years) were enrolled and divided into three groups:38 CKD or ESKD patients with SLE, 40 CKD or ESKD patients without SLE, and 40 healthy controls. For subgroup analyses, CKD (stages3-4) and ESKD (stage 5) patients were considered separately. Those patients meeting the American College of Rheumatology criteria for SLE, while excluding those with infections, malignancies, or other autoimmune disorders were selected. Blood samples were collected, and serum cytokine levels were measured using enzyme-linked immunosorbent assay (ELISA). Statistical analysis was performed using the Kruskal-Wallis and Mann-Whitney U tests, with P ≤ .05 considered significant. RESULTS: CKD patients with SLE showed significantly higher serum levels of IL-1β, TNF-α, and IL-12 compared to CKD patients without SLE and healthy controls (P < .05). IL-6 levels were notably higher in CKD patients compared to ESKD patients, irrespective of SLE status (P < .05). ESKD patients exhibited increased IL-1β, TNF-α, and IL-12 levels, while IL-6 levels were lower than those in CKD patients. CONCLUSION: IL-6 appears to play a crucial role in the pathogenesis of kidney disease, particularly in patients with SLE, and may serve as a therapeutic target. The differential regulation of cytokines in CKD and ESKD suggests that inflammatory pathways vary based on disease stage and the presence of SLE.