The article investigates the crucial roles of oxidative stress and inflammation in the progression of Chronic Kidney Disease (CKD), a condition that poses an increasing global health burden. An imbalance between reactive oxygen species (ROS) and antioxidant defenses leads to mitochondrial damage, which subsequently triggers endothelial dysfunction and promotes kidney fibrosis. CKD symptoms are further exacerbated by inflammation, driven by uremic toxins and cytokine activity. The article highlights NF-κB and Nrf2 as key signaling pathways that regulate these networks. Additionally, it examines how cardiovascular disease, mineral-bone disorder, and cognitive decline emerge as clinical consequences of inflammatory and oxidative tissue damage. Therapeutic strategies for CKD are categorized into three main approaches: antioxidants and anti-inflammatory medications, SGLT2 inhibitors, and bardoxolone methyl. The article also emphasizes non-pharmacological interventions, including behavioral modifications, dietary adjustments, probiotic use, and modulation of the gut microbiota. Finally, it discusses emerging research on biomarker development, precision medicine techniques, and genetic therapies aimed at improving CKD detection, management, and treatment outcomes
Kant et al. (Mon,) studied this question.