Secondary hypertension is defined as hypertension caused by certain underlying diseases and accounts for about 1 to 5% of all hypertensive patients. Its importance lies in the fact that many secondary hypertension, such as primary aldosteronism, pheochromocytoma, renal vascular hypertension, renin secretory tumor, etc., can be cured or significantly improved by surgery or other methods. Early and clear diagnosis can improve the cure rate or prevent the progression of the disease. Causes of secondary hypertension: 1, renal diseases: glomerulonephritis, chronic pyelonephritis, hypertensive syndrome of pregnancy, congenital renal lesions (polycystic kidneys), secondary renal lesions (connective tissue disease, diabetic nephropathy, renal amyloidosis, etc.), renal vascular stenosis. 2.Endocrine diseases: Cushing’s syndrome, pheochromocytoma, primary aldosteronism, adrenal metaplastic syndrome, hyperparathyroidism, anterior pituitary hyperfunction, women taking oral contraceptives for a long time, menopausal syndrome. 3, vascular lesions: aortic stenosis, multiple aortitis. 4, craniocerebral lesions: brain tumor, increased intracranial pressure, traumatic brain injury, brain stem infection. 5, other: plateau disease, erythrocytosis, hypercalcemia, drugs: such as glucocorticoids, sympathomimetic drugs, licorice and so on. The more common secondary hypertension are: 1, renal parenchymal lesions: acute glomerulonephritis, most common in adolescents, with acute onset and history of streptococcal infection, fever, hematuria, edema history, identification is not difficult. Chronic glomerulonephritis is not easy to distinguish from primary hypertension with renal impairment, but a history of recurrent edema, significant anemia, low plasma protein, early onset of proteinuria and relatively mild elevation of blood pressure, and unremarkable fundus lesions are conducive to the diagnosis of chronic glomerulonephritis. Diabetic nephropathy, whether type 1 or type 2, can occur renal damage and hypertension, glomerulosclerosis, glomerular capillary basement membrane thickening as the main pathological changes, early renal function is normal, only a trace of albuminuria, the blood pressure may also be normal; the development of the disease, the emergence of obvious proteinuria and renal insufficiency when the blood pressure increases.ACE inhibitors have a protective effect on the kidney, in addition to lowering the blood pressure, but also can reduce In addition to lowering blood pressure, ACE inhibitors can also reduce proteinuria and slow down the deterioration of renal function. Renal artery stenosis: It can be unilateral or bilateral. The nature of the lesion can be congenital, inflammatory or atherosclerotic, the latter is seen in the elderly, the former two are mainly seen in adolescents. The syndrome should be suspected in all cases of rapidly progressive hypertension or sudden worsening of hypertension with malignant hypertension and ineffective drug therapy. The disease is characterized by moderate to severe elevation of diastolic blood pressure, and a vascular murmur can be heard in the epigastrium or dorsal costovertebral angle on physical examination. High-dose tomographic intravenous pyelography and radionuclide nephrography are helpful in the diagnosis, and renal arteriography can clarify the diagnosis. Treatment includes surgery, percutaneous renal arterioplasty (staring toe), and medications. Surgical treatments include blood flow reconstruction, kidney transplantation, and nephrectomy. Percutaneous renal arterioplasty is easy to perform and has good efficacy, so it is the treatment of choice. Those who are not suitable for the above treatments can only use medication to reduce blood pressure. ACE inhibitors have antihypertensive effect, but may further reduce glomerular filtration rate and deteriorate renal function, especially for bilateral renal artery stenosis should not be applied. Calcium channel blockers have antihypertensive effect and do not significantly affect renal function. Pheochromocytoma: Pheochromocyte tumors such as adrenal medulla or sympathetic ganglion can intermittently or continuously secrete excessive adrenaline and norepinephrine, resulting in paroxysmal or persistent elevation of blood pressure. Any person with obvious blood pressure fluctuation, paroxysmal blood pressure increase with tachycardia, headache, sweating and pallor, ineffective to general antihypertensive drugs, or hypertension with elevated blood glucose, hypermetabolism and other manifestations should be suspected of this disease. Measurement of catecholamine and its metabolite vanillylmandelic acid (VMA) in blood or urine during the period of increased blood pressure, if there is a significant increase, suggests pheochromocytoma. Ultrasound, radionuclide and electronic computed tomography (CT), and magnetic resonance imaging may show the location of the tumor. Most pheochromocytomas are benign and can be surgically removed with good results. About 10% of pheochromocytoma is malignant, and there can be multiple metastatic foci after tumor resection, which can be treated with “‘I-MIBG”. 4.Primary aldosteronism: this disease is caused by adrenal cortex hyperplasia or tumor secreting too much aldosterone. Clinically, it is characterized by long-term hypertension with persistent hypokalemia, and there may be muscle weakness, periodic paralysis, thirst, polyuria, etc. The blood pressure is mostly mild or moderate. Blood pressure is mostly mildly or moderately elevated. Laboratory tests include hypokalemia, hypernatremia, metabolic alkalosis, decreased plasma renin activity, and increased urinary aldosterone excretion. A positive spironolactone (amphotericin) test is of diagnostic value. Ultrasound, radionuclide, and CT can be used for localized diagnosis. Most primary aldosteronism is caused by a single adrenocortical adenoma, and surgical resection is the best treatment. Carcinoma should also be treated by resection, and if there is no metastasis, the efficacy of treatment is also very good. In cases of hyperplasia, major adrenalectomy can be performed, but the results are poor, and medication is usually required. Spironolactone is aldosterone antagonist, which can reduce blood pressure, increase blood potassium and reduce symptoms. 5.Cushing syndrome: It is caused by excessive secretion of glucocorticoids by adrenal cortex tumor or hyperplasia. In addition to hypertension, there are centripetal obesity, full-moon face, buffalo back, purple lines on the skin, increased hair, increased blood glucose and other characteristics, the diagnosis is generally not difficult. 17-hydroxy and 17-keto steroids increase in 24-hour urine, dexamethasone inhibition test and adrenocorticotropic hormone excitability test is positive to help diagnosis. Intracranial pterygoid X-ray, adrenal CT scan and radioiodinated cholesterol adrenal scan can be used for lesion localization. 6. Aortic constriction: Most of them are congenital vascular malformations, and a few of them are caused by polyarteritis. Characterized by increased blood pressure in the upper limbs and no or lower blood pressure in the lower limbs, it is an abnormal phenomenon that the blood pressure in the upper limbs is higher than that in the lower limbs. There may be pulsations and murmurs of collateral circulation arteries in the interscapular region, paraspinal region, axilla or vascular murmurs on abdominal auscultation. Chest radiography may show notching of the ribs caused by erosion of the collateral arteries. Aortography may confirm the diagnosis. Secondary hypertension has a clear etiology and is treated quite differently from the primary. It is important to familiarize oneself with the characteristics of the various types of secondary hypertension described above, especially in patients under the age of 40 who present with hypertension.