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.