Small arteriolar vitreous lesions are caused by systemic hypertension and are ranked as the second most common disease causing end-stage renal failure in Western countries (about 25%), and the incidence is increasing in China. This disease can be divided into 2 types: benign small artery renal sclerosis and malignant small artery sclerosis. Benign small artery nephrosclerosis is caused by long-term uncontrolled benign hypertension, the higher the blood pressure and the longer the duration, the more severe the lesion. The arterial lesions are mainly glassy lesions in the walls of the small arteries entering the bulb, and thickening of the intima of the walls of the interlobular and arcuate arteries, which cause ischemic renal parenchymal damage. The causes of malignant small arterial sclerosis are the direct effect of increased blood pressure; the action of renin, angiotensin and microvascular intravascular coagulation. When blood pressure is significantly increased the tension of the vessel wall increases, causing damage to the vascular endothelium, increased permeability, penetration of fibrin and other components of the blood into the vessel wall, producing pathological changes in the small arteries. In malignant small artery nephrosclerosis, blood levels of renin and angiotensin are elevated, suggesting a role in the pathogenesis. When hypertension causes renal vascular injury, it makes renal tissue significantly ischemic, activating the renin and angiotensin system and increasing renin and angiotensin production, which in turn exacerbates elevated blood pressure and renal vascular lesions and aggravates renal ischemia, thus constituting a vicious circle. The direct damaging effect of the vascular wall during hypertension activates the coagulation system, causing platelet coagulation and fibrin deposition in the tubular wall and stimulating smooth muscle cell hypertrophy and hyperplasia. At the same time, the red blood cells in the blood are easily damaged and destroyed when passing through the diseased vessels, thus causing intra-microvascular coagulation and local intravascular hemolysis and aggravating the damage to the small renal vessels. In malignant small artery nephrosclerosis, renal blood flow and GFR are significantly decreased, and the intrarenal blood flow distribution is significantly decreased by renal cortical blood flow. Extensive vascular lesions can cause glomerular ischemia, atrophy, and fibrosis.