Renal fibrosis is a defining feature of chronic kidney disease (CKD), marked by the excessive accumulation of extracellular matrix (ECM) that leads to scarring and progressive loss of kidney function. Affecting an estimated 10–14% of the global population, CKD often advances silently until it culminates in end-stage renal failure, a life-threatening condition requiring dialysis or kidney transplantation. The development of renal fibrosis is driven by chronic inflammation, activation of myofibroblasts, epithelial-to-mesenchymal transition (EMT), and ECM buildup, all of which contribute to irreversible tissue damage. Diabetes and hypertension are the most common underlying causes of CKD, with glomerulosclerosis and tubulointerstitial fibrosis emerging as key consequences of disrupted balance between ECM production and degradation. Despite its clinical significance, there are currently no effective USFDA approved therapies that are specially targeted to prevent or reverse the progression of renal fibrosis, highlighting the urgent need for early diagnosis and targeted interventions.