Renal hypertension

 What is the cause of renovascular hypertension and what are its clinical characteristics?

The main causes of renovascular hypertension are as follows

(1) Renal artery lesions: 1. Atherosclerotic plaque of renal artery intima; 2. Fibrous tissue hyperplasia of renal artery; 3. Nonspecific Takayasu arteritis; 4. Congenital renal artery abnormalities; 5. Renal aneurysm, acquired or congenital; 6. Nodular periarteritis; 7. Renal artery embolism; 8. Renal artery or aberrant renal artery thrombosis; 9. Syphilitic renal arteritis; 10. Thrombotic renal arteritis; 1 1. Renal artery injury, trauma or surgical trauma; 12. Renal pedicle distortion; 13. Renal arteriovenous fistula; 14. Abdominal aorta coarctation with or without renal artery obstruction.

(2) Renal artery compression: 1. Abdominal aortic aneurysm; 2. Other mechanical factors, such as tumor, cyst, hematoma, fibrous band, paraaortic lymphadenitis and chronic inflammation around renal artery.

Renovascular hypertension in children is mostly caused by congenital renal artery abnormalities; young people are often caused by renal artery fibrous tissue hyperplasia, non-specific Takayasu arteritis; more than 50 years old patients, renal atherosclerosis is the most common cause.

What is the cause of renal parenchymal hypertension and what are its clinical characteristics?

The diseases causing renal parenchymal hypertension are as follows:

1. Primary glomerulonephritis, such as acute glomerulonephritis, progressive glomerulonephritis and chronic glomerulonephritis; 2. Lupus nephritis is more common in secondary glomerulonephritis; 3. Polycystic kidney; 4. Congenital renal hypoplasia; 5. Chronic pyelonephritis; 6. Radioactive nephritis; 7. Renal tuberculosis; 8. Giant hydronephrosis; 9. Renal tumor; 10. Renal calculus; 11. Renal amyloidosis; 12. Renal medullary cystosis.

Almost every kind of kidney disease can cause hypertension, whether unilateral or bilateral renal parenchymal disease. Usually glomerulonephritis, lupus nephritis, polycystic kidney, congenital renal hypoplasia and other diseases, if the lesion is more extensive and accompanied by vascular disease or renal ischemia is more extensive, often accompanied by hypertension. For example, diffuse proliferative glomerulonephritis often due to extensive lesions, severe renal ischemia, so that hypertension is very common; conversely, small lesions, focal proliferative glomerulonephritis rarely occur hypertension. Renal tuberculosis, renal calculi, renal amyloidosis, hydronephrosis, simple pyelonephritis, renal medullary cystosis and other lesions with renal tubulointerstitial damage are less likely to produce hypertension. But once these diseases develop to affect glomerular function, hypertension often occurs. Therefore, the incidence of renal parenchymal hypertension is closely related to glomerular function. The incidence of hypertension in end-stage renal failure can reach 83%.

What is the pathogenesis of renal hypertension?

The pathogenesis of renal hypertension mainly includes the following two points

* (1) easy to rely on hypertension: about 90% of renal hypertension is caused by water sodium retention and blood volume expansion. When the renal parenchymal lesion causes the kidneys to lose the amount of * (excess) water and salt contained in the excretory diet, it will cause water and sodium to remain in the body and cause excessive blood volume to cause hypertension. As long as there is mild renal insufficiency, this mechanism will appear. Plasma renin and angiotensin Ⅱ (a Ⅱ) levels are usually low in these patients. Hypertension can be reduced by limiting the amount of water and salt or removing too much water and salt through dialysis.

(2) Renin dependent hypertension: renal artery stenosis and 10% of renal parenchymal hypertension are caused by increased renin angiotensin aldosterone. Diuresis and dehydration can not control this kind of hypertension. On the contrary, the decrease of renal blood flow after diuresis and dehydration often leads to the increase of renin secretion and the increase of blood pressure. It is suggested that the renin angiotensin system plays an important role in the pathogenesis of this type of hypertension.

In fact, the pathogenesis of hypertension is much more complex than this simple classification. Because some patients' hypertension can't be explained by volume overload or excessive renin. At the same time, these two kinds of pathogenesis are interrelated. Increased blood volume often inhibits renin-angiotensin system, while salt loading greatly increases the sensitivity of a Ⅱ. The pressor effect of a Ⅱ mainly depends on the stability of sodium internal environment. Therefore, renal hypertension is divided into two categories, mainly to help understand and study the pathogenesis of hypertension, so as to find an effective way to reduce blood pressure.

Which diseases should renal hypertension be differentiated from?

Renal hypertension should be differentiated from the following diseases:

(1) Endocrine hypertension: in endocrine diseases, hypertension occurs in hypercortisolism, pheochromocytoma, primary aldosteronism, hyperthyroidism and menopause. However, the diagnosis can be made according to the history of Endocrinology, special clinical manifestations and endocrine test.

(2) Vascular disease: congenital coarctation of aorta, multiple Takayasu arteritis can cause hypertension. It can be differentiated according to the blood pressure of the upper and lower extremities, as well as pulseless disease.

(3) Intracranial disease: some encephalitis or tumor, intracranial hypertension, etc. often have hypertension. The nervous system symptoms of these patients are often prominent, which can be diagnosed by detailed examination of the nervous system.

(4) Other secondary hypertension: such as pregnancy poisoning and some rare diseases can appear hypertension, such as renin secreting tumor.

(5) Primary hypertension: the onset age is relatively late, may have family history, after excluding secondary hypertension can make a diagnosis.