As a general rule, at the beginning of the
change in pressure alter renal function, has brought about the change in
structure. By the time the structural change will affect the functionality. And
finally when the original structure is broken, the function will decline.
Hypertensive nephropathy occurs in the majority of hypertensive patients not
treated.
The first stage does not change anything,
MLCT slight increase.
Following stages: Signs persistent
microalbumin in urine is an early stage of hypertensive renal disease.
Glomerular filtration rate in normal.
If untreated patients with microalbuminuria
will progress to clinical proteinuria (urinary albumin> 300 mg / mg
creatinine or> 300 mg / 24 hours). Once clinical proteinuria, glomerular
filtration rate will decrease rapidly, kidney failure will become increasingly
clear.
Currently hypertensive renal disease is
second leading cause of diabetes causes of end-stage renal disease should hemodialysis,
peritoneal dialysis or kidney transplantation cycle in many countries. Compared
with end-stage chronic kidney disease due to other causes, patients with
chronic end-stage renal failure due to hypertension had more cardiovascular
risk factors other than clear and mortality rates are higher. Preventing the
progression of kidney damage is one of the main goals when treating patients
with hypertension. Hypertension is a motivating factor in kidney damage
progresses faster. Research MDRD (Modification of Diet in Renal Disease) in the
kidney due to many different reasons to see patients with controlled blood
pressure was positively reduced glomerular filtration rate slower than patients
with blood pressure was maintained at normal levels. When aggregating data from
nine clinical trials evaluating the effects of antihypertensive treatment on
kidney function, the authors found that people with chronic kidney disease have
uncontrolled blood pressure (> 140/90 mmHg) decreased glomerular filtration
rate of 12 ml / min / year, whereas those with chronic kidney disease have high
blood pressure is 130/85 mm Hg under control decreased glomerular filtration
rate is only about 2 ml / min / year (equivalent to the reduction of physiological).
Change glomerular filtration rate in patients
with renal hypertension when autoregulation mechanism in the kidney (renal
autoregulation) no longer works. Normal renal autoregulation of renal blood
flow and keep the pressure in the glomerular stable when the average blood
pressure change in a wide range from 80 to 160 mm Hg. The mechanism of the
self-regulate vasomotor reflexes of arterioles to (afferent arteriole): When
the average reduction in blood pressure, arteriolar dilation to, whereas the
average increase in blood pressure, arteriolar to co back. The feedback
mechanism tubules - glomeruli (tubuloglomerular feedback) is the change in tone
of arterioles to meet with tubular NaCl concentration away. In addition, the co
arterioles go (efferent arteriole) mediated angiotensin II also contributes to
maintain the pressure in the glomerular renal perfusion pressure decreased.
Chart 1 below shows the relationship between average blood pressure body with
glomerular filtration pressure, factors determining the glomerular filtration
rate. Street performers self-regulate pressure in the glomeruli of normal,
chronic hypertension who have normal kidney function and chronic hypertension
associated with chronic kidney disease
In patients with chronic hypertension, due to
endothelial dysfunction and structural changes of the renal arterioles,
glomerular pressure starts to decrease at a rate higher than 80 mmHg and
started to increase at a rate higher than 160 mmHg. If performing the change of
pressure in accordance with changes in glomerular average blood pressure on a
chart, we can see in people with chronic hypertension phenomenon curve
"misses to the right." Particularly in patients with hypertension
associated with chronic renal injury, self-conditioning system disorders
glomerular arterioles before losing the ability to stretch. In this the
pressure in the glomerular changes almost parallel with the average blood
pressure.
The consequence of the reduction in
glomerular pressure is decreased glomerular filtration rate, expressed as
increases in serum creatinine. Increases in serum creatinine particularly
common in patients with hypertension associated with chronic kidney disease. In
the first phase the reduced glomerular filtration rate nature hemodynamic not
reflect the reality of kidney damage and is usually transient. Glomerular
filtration rate will be restored and improved if better blood pressure control
improves the structure and function in renal arterioles and shifting
autoregulation curve of normal position. If high blood pressure continues to
increase, the damage increases renal fibrosis. clinical proteinuria appears
constant and glomerular filtration rate will decrease rapidly. The higher the
blood pressure, glomerular filtration rate decreases more. Finally, renal
fibrosis completely lost filtering function and required replacement therapy.
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