( A) causes
Variety of renal parenchymal disease can cause high blood pressure ,
hypertension, renal parenchymal disease incidence differ somewhat different (
Table 1 ) .
1 can cause hypertension, renal disease , including unilateral reflux
nephropathy , chronic pyelonephritis , hydronephrosis and renal adenocarcinoma ,
if detected ipsilateral renal vein renin levels high , early excision may be
suffering from kidney cure or significantly improve blood pressure . Congenital
absence of one kidney ( renal agenesis ) more common in patients with
hypertension , but the day after unilateral nephrectomy ( removal of kidney
disease or kidney transplant donor ) but did not increase the risk of
hypertension , the mechanism is not clear.
2 high blood pressure can cause a lot of bilateral renal parenchymal disease
, including the original , secondary glomerular diseases , chronic interstitial
nephritis, adult polycystic kidney disease and so on. In general , the original
, hypertension secondary to glomerular disease incidence in chronic interstitial
nephritis, and adult polycystic kidney disease , while in the former , secondary
glomerular diseases , pathology showed proliferation and ( or ) hardening
performers highest rates of hypertension . In addition, no matter what kidney
disease when it occurs with impaired renal function , the incidence of
hypertension is increased, the literature, about 90% of end-stage renal disease
patients with hypertension.
( B) the pathogenesis
Acute renal parenchymal disease causes high blood pressure is the main
mechanism of sodium retention , increased blood volume , blood pressure
decreased diuretic often make even normal . The pathogenesis of hypertension,
chronic renal disease , but more complicated by a variety of factors .
Factor 1 . Cause sodium retention , increased blood volume
( 1 ) leads to increased blood volume : there are factors that can cause
sodium retention : ① GFR (glomerular filtration rate, GFR) decreased sodium and
water excretion decreased ; ② renin - angiotensin - aldosterone system
activation , aldosterone promote distal tubule and collecting duct sodium
reabsorption ; ③ sympathetic nervous system activation , and promote proximal
tubular reabsorption of sodium ; ④ NO (nitric oxide, NO) decreased production ,
tubular natriuresis decrease ; ⑤ renal function insufficiency leading to insulin
resistance, increased insulin levels , stimulation of the sodium pump (Na-K-ATP
enzyme ) increased proximal tubular reabsorption of sodium . Sodium retention
can lead to a significant volume of hypertension .
( 2 ) result in increased vascular resistance : the following mechanisms may
lead to an outer peripheral and renal arteries, vascular resistance increased :
① renin - angiotensin - aldosterone system activation , activation of the
sympathetic nervous system and endothelin synthesis, both stimulate
vasoconstriction ; ② NO decreased production , antagonize vasoconstrictor
factors weakened ; ③ GFR decline resulted in increased secretion of parathyroid
hormone , quinoline Pakistan due to the release of endogenous extracellular
volume expansion stimulated by parathyroid hormone and quinoline Pakistan can
increase the concentration of intracellular Ca2 promote vasoconstriction and
increase the muscle wall of the vasoconstrictor factor sensitivity ; ④ insulin
resistance, high insulin levels stimulate vascular smooth muscle hypertrophy ,
vascular response enhancement, wall thickening , luminal narrowing, increased
vascular resistance. These factors could lead to resistance to hypertension.
In renal hypertension , the mere volume of hypertension or hypertension pure
resistance are rare , most patients department two kinds of risk factors
coexist. Compared with essential hypertension, renal hypertension volume factors
often more obvious.
Can be learned from the above description , regardless of volume or
resistance of hypertension , are associated with many related neurohormonal
factors involved , briefly summarized in Table 2 .
2 factors that lead to high blood pressure
( 1 ) the renin - angiotensin - aldosterone system (rennin-angiotensin
aldosterone system, RAAS) activation : a lot of information has been confirmed
in the occurrence and development of RAAS plays an important role in renal
hypertension , renal parenchymal disease missing the blood can lead to RAAS
activation. Angiotensin Ⅱ (angiotensin Ⅱ, A Ⅱ) can directly stimulate
vasoconstriction , but also by increased central sympathetic activity , and
acting on the sympathetic nerve endings to promote the release of catecholamines
, further vasoconstriction ; aldosterone increases the distal tubule and
collecting duct sodium reabsorption , increased sodium retention . Thus , RAAS
activation involved in the resistance of both , but also to participate in the
volume of hypertension .
( 2 ) enhanced sympathetic activity : Sympathetic also play an important role
in the pathogenesis of renal hypertension . When the renal afferent renal
parenchymal disease through sympathetic reflex (afferent renal reflexes)
activation , A Ⅱ will also benefit from an increase in the central and
peripheral increase its activity. The sympathetic nervous system activation
stimulated vasoconstriction, increased vascular resistance ; promote proximal
tubular reabsorption of sodium , increased blood volume, and therefore able to
participate in both the resistance and the volume of hypertension . Activation
of the sympathetic nervous system and renal vasoconstriction can , decreased
renal blood flow and stimulate
Renin secretion, further weight gain RAAS activation hypertension .
( 3 ) the release of endogenous digitalis- like substance : with digitalis
antibodies cross from the reaction of endogenous digitalis -like substance
(endogenous digitalislike substance, EDIS) has the following characteristics :
inhibition of Na-K-ATP enzyme , natriuresis . When renal parenchymal disease
causes extracellular volume expansion , which can reflect the brain to stimulate
the hypothalamus to release EDIS, inhibition of proximal tubular epithelial cell
Na-K-ATP enzyme , reducing sodium reabsorption , since natriuresis effect .
However , on the other hand the inhibition of vascular smooth muscle EDIS
Na-K-ATP enzyme , increased intracellular sodium concentration , reduced sodium
transmembrane gradient, Na / Ca2 exchange and reduced voltage-dependent Ca2
channels depolarization within the cytoplasmic Ca2 therefore increase , which
promotes the resistance of hypertension .
( 4 ) ET : ET is the strongest ever found in vivo vasoconstrictor peptide ,
it is possible through endocrine pathways , as well as autocrine and paracrine
pathways play a role. Endothelin stimulates vasoconstriction ; promote RAAS
activation ; reduce renal blood flow and GFR, reduce urinary sodium excretion.
Therefore , it may be involved in the pathogenesis of renal hypertension from
both resistance and volume .
( 5 ) arginine vasopressin : arginine vasopressin to normal body and little
effect on blood pressure in patients with essential hypertension , but clinical
trials have indicated that chronic renal failure who applied to arginine
vasopressin antagonists can effectively decrease blood pressure , suggesting
that arginine vasopressin vasoconstrictor effect by those involved in renal
hypertension . However, this observation is certainly still need more research
and a clear mechanism.
( 6 ) reduced antihypertensive factor : renal factors can produce a variety
of blood pressure , such as prostaglandin E2 and I2, bradykinin ( distal renal
tubular epithelial cells kallikrein , and then the plasma kinin into bradykinin
Original ) , atrial natriuretic peptide, brain natriuretic peptide , NO and
medulla buck fat and so on. As former Syria , renal parenchymal disease N0
decreased production , antagonize vasoconstriction diminished capacity , but
also to reduce NO reduce renal tubular sodium excretion , increased sodium
retention , and therefore it from participating in both resistance and volume of
hypertension . However, they have not been involved in these other
antihypertensive factor conclusive evidence of renal parenchymal hypertension
.
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