Fibrous infarction of the small renal artery is a symptom of primary malignant hypertension. So, what can cause patients with small renal arteries with fibrous infarction? The following is a brief introduction: 1, the direct effect of increased blood pressure: when the blood pressure is significantly elevated, the tension of the vascular wall increases, causing damage to the vascular endothelium, increased permeability, and the infiltration of fibrin and other components of the blood into the vascular wall, resulting in pathological changes of the small arteries. 2, the role of renin and angiotensin: in malignant small artery nephrosclerosis, the level of renin and angiotensin in the blood is increased, suggesting that they play a role in the pathogenesis. When hypertension causes renal vascular injury, it makes the renal tissue obviously ischemic, activating the renin and angiotensin system, which increases the production of renin and angiotensin, which in turn aggravates 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.