NF-ΚB–MEDIATED INFLAMMATION AS A MECHANISM OF TUBULAR INJURY IN HYPERURICEMIA

Hyperuricemia is increasingly recognized as a significant risk factor for renal tubular injury. Recent studies highlight that elevated uric acid levels can activate NF-κB signaling, triggering pro-inflammatory cytokine production, oxidative stress, and fibrotic mediator release in renal tubular cells. This NF-κB–mediated inflammation plays a central role in tubular cell apoptosis, fibrosis, and progressive renal dysfunction, independent of urate crystal deposition. Understanding the molecular mechanisms linking hyperuricemia to tubular injury provides insights for potential therapeutic interventions. Targeting NF-κB signaling, alongside urate-lowering therapies and antioxidants, may reduce inflammation and preserve renal tubular function. This study emphasizes the clinical and molecular relevance of NF-κB–mediated pathways in hyperuricemia-associated kidney damage.高尿酸血症（Hyperuricemia）日益被认为是肾小管损伤的重要危险因素。近期研究表明，血尿酸水平升高可激活核因子κB（NF-κB）信号通路，进而诱导肾小管细胞产生促炎细胞因子、引发氧化应激并释放纤维化介质。这种由核因子κB介导的炎症反应在肾小管细胞凋亡、纤维化及进行性肾功能不全中发挥核心作用，且该过程不依赖于尿酸盐晶体沉积。阐明高尿酸血症与肾小管损伤之间的分子机制，可为潜在的治疗干预手段提供理论依据。靶向核因子κB信号通路，联合降尿酸治疗与抗氧化剂，或可减轻炎症反应并保护肾小管功能。本研究着重阐述了核因子κB介导的通路在高尿酸血症相关性肾损伤中的临床与分子关联意义。