1, volume-dependent hypertension: After renal parenchymal damage, the function of the kidney to handle water and sodium is reduced, and water and sodium retention can occur. The blood volume can be expanded, and hypertension can occur. It can also cause an increase in the content of water and sodium in the smooth muscle of blood vessels, thickening of blood vessel walls, decreased elasticity, increased resistance of blood vessels and responsiveness to catecholamines and increased affinity of angiotensin type 2 for vascular receptors to increase blood pressure. 2, renin-dependent hypertension: the pathogenesis of renal artery stenosis, decreased intrarenal perfusion, renal parenchymal disease and renin-secreting cell tumors can cause the release of large amounts of renin from parabellular cells, causing an increase in angiotensin 2 blood, the systemic small artery wall contraction, and cause an increase in blood pressure, in turn, renin and angiotensin 2 can cause increased secretion of aldosterone, resulting in water and sodium retention, resulting in increased blood volume, and increase blood pressure. In turn, renin and angiotensin 2 can increase secretion of aldosterone, leading to water and sodium retention, increasing blood volume, and increasing blood pressure. Secondly, after renal parenchymal damage, the release of kinin release enzyme and prostaglandin decreases, and these vasodilatory substances decrease, which is also an important factor in the formation of hypertension. Therefore, hypertension is the most common clinical manifestation of renal disease. However, renal vascular hypertension can be cured by surgery and is generally better treated in the medium to long term.