Renal hypertension is mainly due to the secretion of renin from the parabolic cells of the glomerular arteries, which causes the synthesis of angiotensin and increases the peripheral vascular resistance due to the contraction of small arteries and smooth muscles throughout the body, and stimulates the secretion of aldosterone from the adrenal cortex, which causes the retention of water and sodium, resulting in an increase in blood volume and an increase in blood pressure. The onset of renal hypertension is usually slow, with no obvious symptoms in the early stages, and the blood pressure may be found to be elevated by chance after several years of good self-consciousness. In the case of persistent aggravation of renal atherosclerosis, some early symptoms may gradually appear, including headache and fatigue, palpitations, and tinnitus. As the kidney problem worsens. Proteinuria, hematuria and even renal failure will appear after the kidney function is damaged. Blood pressure will gradually rise, from an initial temporary increase, gradually becoming more pronounced and persistent. There is a significant difference between daytime and nighttime blood pressure levels. The symptoms of renal hypertension become more pronounced in the presence of a continuous decrease in renal perfusion, a decrease in the concentration of sodium in the renal tubules, stress, and cold stimulation. It can cause damage to the corresponding organs of the heart and brain. Ultimately, it will aggravate the failure of kidney function and cause the serious problem of uremia.