Background: The defining characteristic of systemic arterial hypertension, commonly known as hypertension, is persistently high blood pressure (BP) in the systemic arteries. One common approach to express blood pressure is the ratio of systolic blood pressure to diastolic blood pressure. Systolic blood pressure is the force that the blood applies to the arterial walls when the heart contracts, while the diastolic BP is the pressure when the heart relaxes. Depending on the method of measurement, certain BP cutoffs indicate hypertension. It is generally accepted that chronic kidney disease (CKD) will advance more quickly as a result of elevated systemic blood pressure and that accelerated and malignant types of hypertensions can quickly cause permanent kidney failure. On the other hand, it continues to be debated whether modest to moderate increases in systemic blood pressure frequently cause CKD and subsequently end-stage renal disease (ESRD). Most hypertension patients experience mild-to-moderate hypertensive nephrosclerosis. Nevertheless, when BP values are uncontrolled for a prolonged period of time or kidney disease is present, the proportion of people who develop ESRD drastically rises. The chronological sequence of events (i.e., whether CKD or hypertension occurred first) in the majority of cases of concomitant hypertension and CKD cannot be determined. Hypertensive nephrosclerosis involves hyalinization and sclerosis of interlobular and afferent arterioles, together with glomerular and tubulointerstitial compartments fibrosis. Blood is supplied to afferent arterioles under higher pressure because of ageing and hypertension-related arterial stiffness. Early on, post glomerular vascular hypoxia caused by glomerular ischemia results in primarily monocytic/macrophagic inflammation and epithelial–mesenchymal transition (EMT). For many years, it was believed that hypertensive kidney disease was a condition that only affected the afferent arterioles and glomeruli, and that the pathogenic mechanisms causing the kidney damage were mechanical stress brought on by high blood pressure, RAAS stimulation, and activation of local fibroblasts. Epithelial-mesenchymal transition, podocyte loss, and tubulointerstitial fibrosis have so far been identified as the primary pathways for the development of cytoprotective treatment approaches.