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.
~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.