Small arteriovenous vitreous lesions of the innominate arteries can be divided into 2 types: benign small arteriovenous nephrosclerosis and malignant small arteriovenous sclerosis. The following is an introduction to the causes of these two diseases. Benign small artery renal sclerosis is caused by long-term uncontrolled benign hypertension, the higher the blood pressure and the longer it lasts, 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-media of the walls of the interlobular and arcuate arteries, which cause ischemic renal parenchymal damage. Malignant small arterial sclerosis 1, the direct effect of increased blood pressure: when the blood pressure is significantly increased the tension of the vessel wall increases, making the endothelial cells of the blood vessels damaged, permeability is enhanced, fibrin and other components of the blood penetrate into the vessel wall, producing pathological changes in the small arteries. 2, the role of renin and angiotensin: in malignant small arterial nephrosclerosis blood renin and angiotensin levels rise, suggesting that they play a role in the pathogenesis. When hypertension causes renal vascular injury, it makes renal tissue obviously ischemic, activates renin and angiotensin system, which increases renin and angiotensin production, which in turn exacerbates the elevated blood pressure and renal vascular lesions, aggravating renal ischemia, thus constituting a vicious circle. 3, intra-microvascular coagulation: the direct damage to the blood vessel wall during hypertension acts to activate the coagulation system, causing platelet coagulation and deposition of fibrin in the tube wall, 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.