In recent years, researches have proven that Angiotensin- converting enzyme inhibitor is effective in reducing blood pressure. Clinical practices also show that calcium antagonist can also effectively reduce blood pressure and thus alleviate the high blood perfusion state. In addition, calcium antagonist is also helpful with reducing oxygen consumption and blocking the assembly of soterocyte. This medicine can also reduce the incidence of calcium deposition on renal mesenchyme. By this, the purpose of reducing renal damage and stabilizing renal function can be achieved.
Clinical practices have proven that long-term adoption of calcium antagonist will not lead damages to glomerulus. what is more, calcium has no preventing protein leakage effect.
For hypertension Immunotherapy from excessive secretion of renin, beta receptor antagonist is of great help. Corresponding medicines include Metoprolol and Atenolol reduce the secretion of renin but will neither impair blood inflow to the kidneys nor declining glomerular filtration rate. However, patients must understand that these drugs are of low lipid solubility and they are excreted out of the body through the kidneys, so for patients with renal insufficiency, they should pay much attention on adopting proper medicine dosage and prolonging medicine using intervals.
Why patients with Chronic Nephritis are more vulnerable to hypertension
Hypertension that Immunotherapy from Chronic Nephritis accounts for 5%--10% of all adult hypertension. Nephritic hypertension can be the result of increased blood volume and the excessive secretion of renin.
Pathological changes of kidneys give rise to body fluid retention, which correspondingly increase the blood volume and as a result increases blood pressure. The difficulty in sodium excretion is the main reason of this type of high blood pressure.
Pathological changes of renal cortex and renal vessels will give rise kidney blood insufficiency which stimulates renal cells of goal artery to secrete renin. Renin is a kind of hydrolysis protease which can transform liver produced proangiotensin into angiotensin Ⅰ, which latterly will be transformed by angiotensin converting enzyme into angiotensin II. Angiotensin II is of high activity and can effectively contract vessels. In addition, angiotensin II enhance the secretion of aldosterone which is a kind of hormone that adjusts blood volume. Excessive secretion of aldosterone promotes the water and sodium reabsorption ability of renal tubules. And the excessive absorption of water and sodium in turn aggravates blood volume and the condition of hypertension.
~Hypertension Caused by Chronic Kidney Disease(ckd)
Details of Immunotherapy
2011-06-13 18:02
Under the condition of Chronic Nephritis, remaining nephrones are in a state of compensation, which means that high blood perfusion exists in the kidney. And the general hypertension will only aggravate this state.
In recent years, researches have proven that Angiotensin- converting enzyme inhibitor is effective in reducing blood pressure. Clinical practices also show that calcium antagonist can also effectively reduce blood pressure and thus alleviate the high blood perfusion state. In addition, calcium antagonist is also helpful with reducing oxygen consumption and blocking the assembly of soterocyte. This medicine can also reduce the incidence of calcium deposition on renal mesenchyme. By this, the purpose of reducing renal damage and stabilizing renal function can be achieved.
Clinical practices have proven that long-term adoption of calcium antagonist will not lead damages to glomerulus. what is more, calcium has no preventing protein leakage effect.
For hypertension Immunotherapy from excessive secretion of renin, beta receptor antagonist is of great help. Corresponding medicines include Metoprolol and Atenolol reduce the secretion of renin but will neither impair blood inflow to the kidneys nor declining glomerular filtration rate. However, patients must understand that these drugs are of low lipid solubility and they are excreted out of the body through the kidneys, so for patients with renal insufficiency, they should pay much attention on adopting proper medicine dosage and prolonging medicine using intervals.
Why patients with Chronic Nephritis are more vulnerable to hypertension
Hypertension that Immunotherapy from Chronic Nephritis accounts for 5%--10% of all adult hypertension. Nephritic hypertension can be the result of increased blood volume and the excessive secretion of renin.
Pathological changes of kidneys give rise to body fluid retention, which correspondingly increase the blood volume and as a result increases blood pressure. The difficulty in sodium excretion is the main reason of this type of high blood pressure.
Pathological changes of renal cortex and renal vessels will give rise kidney blood insufficiency which stimulates renal cells of goal artery to secrete renin. Renin is a kind of hydrolysis protease which can transform liver produced proangiotensin into angiotensin Ⅰ, which latterly will be transformed by angiotensin converting enzyme into angiotensin II. Angiotensin II is of high activity and can effectively contract vessels. In addition, angiotensin II enhance the secretion of aldosterone which is a kind of hormone that adjusts blood volume. Excessive secretion of aldosterone promotes the water and sodium reabsorption ability of renal tubules. And the excessive absorption of water and sodium in turn aggravates blood volume and the condition of hypertension.
