FIBROBLAST GROWTH FACTOR 23–KLOTHO AXIS DYSFUNCTION IN CHRONIC KIDNEY DISEASE: MOLECULAR MECHANISMS OF INFLAMMATION, MINERAL IMBALANCE, AND CARDIOVASCULAR REMODELING

Chronic kidney disease is a progressive and irreversible clinical syndrome characterized by the gradual loss of nephron function, leading to disturbances in fluid balance, electrolyte homeostasis, endocrine regulation, and metabolic stability. As renal function declines, patients develop a complex constellation of systemic complications collectively described as chronic kidney disease–mineral and bone disorder, cardiovascular remodeling, chronic inflammation, oxidative stress, and progressive interstitial fibrosis. Cardiovascular mortality remains the leading cause of death in individuals with advanced renal impairment, far exceeding the risk observed in the general population. Among the molecular mechanisms implicated in this excessive cardiovascular burden, dysregulation of the fibroblast growth factor 23–klotho signaling axis has emerged as a central pathophysiological driver..