study on hemodynamic index of kidney arteries and glomerular filtration rate in essential hypertension patients

MINISTRY OF EDUCATION AND TRANING MINISTRY OF NATIONAL DEFENCE
VIETNAM MILITARY MEDICAL UNIVERSITY
NGUYỄN VĨNH HƯNG
STUDY ON HEMODYNAMIC INDEX OF KIDNEY ARTERIES
AND GLOMERULAR FILTRATION RATE
IN ESSENTIAL HYPERTENSION PATIENTS
Specialist: Nephrology-Urology
Code: 62.72.01.46
Epitomize of PhD thesis
Hanoi - 2014
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Research completed in:
VIETNAM MILITARY MEDICAL UNIVERSITY
Supervisor I: AssProf. PhD HA HOANG KIEM
Supervisor I: AssProf. PhD DINH THI KIM DUNG
Scientific reviewer I: Ass.Prof TRAN VAN CHAT
Scientific reviewer II: Ass.Prof DOAN VAN DE
Scientific reviewer III: AssProf. PhD NGUYEN VAN QUYNH
Thesis will be presented in university examiner assembly
In Vietnam military medical university
At hour min, day month year 2014
Find thesis in
1. National library
2. Vietnam military medical university
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INTRODUCTION
Hypertension (HTA) is cause and consequences of CKD. Renal
failure is severe of HTA and affects quality of life’s patients and is the
heavy burnde of social. USRDS 2005 showed 27% FSRD caused by

HTA, HTA is 2
nd
caused less than diabetes 51%. WHO warned HTA in
Vietnam will be most important cause of ESRD in near future.
HTA lead increasing of blood flow of kidney and intragromerular
pressure increase. Belong the time, normal structure of gromeruli will be
destroyed, sclerosis and kidney function decreased and the end ESRD.
HTA destroyed all kinds of kiney arteries by the longtime hype pressure.
This procedure is dangerous because it hell is “silent”. Signes appearred
late, when loss kidney function.
Doppler ultrasound is non-invasive intervention for diagnose
follow up kidney arteries disorder. This technique help find out early
injury caused by HTA. There are many research about disease caused by
HTA. Therefore need more research in hemodynamic kidney arteries
and gromerular filtration rate. Information received help diagnose early,
prevent kidney complication of HTA.
OBJECTIF
1. Study on hemodynamic index (HI)(speed of blood flow, blood flow
volume, resistance index, pulsasitive index); Plasma renin concentration
(PCR) and gromerular fitration rate (GFR) in essential HTA with
negative macroalbuminuria.
2. Relationship of blood flow volume (FV) of kidney arteries, GFR with
PRC, and anothers hemodynamics index.
NEWCONTRIBUTION OF THESIS
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- Result received reconfirms HI of kidney arteries, GFR depend on
HTA situation: Stage of HTA, time of HTA.
- Warning clinical physics evaluate completely, systematic, chronology
HI, GFR, PCR in essential patients to prevent renal injuries.

CONTENT OF THESIS
Thesis have 124 pages: Introduction 2 pages, Chapter 1:
Background 24 pages, Chapter 2: Subjects and method 15 pages,
Chapter 3: Result 33 pages, Chapter 4: Discusion 29 pages.
Thesis has 44 tables, 3 schemas, 3 images. References 162: in
Vietnamese 26 and 146 in English.
Chapter 1
BACKGROUND
1.1. Kidney injuries caused by HTA
Early, changing of function passed in the longtime recurred if
right treated. Later, sclerosis accelerated and dimension of kidney
decreases cause ERSD.
GFR in early time maintain with low FV (flow volume) but later
GFR decreased and ESRD at the end.
All of kidney arteries injured but mostly in afferent arteries. The
character of histological injuries’ is intimae artery and endothelia
destruction sclerosis, necroses all of the arteries.
1.2. GFR disorder in HTA
Theory, changing of pressure lead changing function, later
structure destroyed, belong the time abnormal struction decreases
function. Actually, most of CKD hypertensions aren’t treated. In early
time of HTA, GFR in normal ranger or increase lightly. Late, when MAU
appeared, GFR in normal range. If patient aren’t under good HTA
controlled; Microalbumin or clinical protein in uria appeared, GFR
decrease significally, clinical signs of renal failure more severe.
GFR loss in HTA patient caused by renal auto regulation system
dysfunction. Auto regulation contraction of afferent arteries and refection
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tubulo-glomerular system disordes. HTA chonic patient from epithelial

dysfunction and structural arteries destroyed. Intragromerular pressure
decreased with blood pressure higher than 80mmHg and increase with BP
higher than 160mmHg.
1.1 . Renal artery interventional method
- Direct method:
+ Ultrasound color Doppler
+ Digital angiography
+ MRI
- Indirect
+ Intravenous urography, image nuclear
+ Biochemical test
1.2 . Researches hemodynamic index and GFR in HTA patients in Vietnam
and global.
MDRD research showed CKD patient have slower decreased of GFR if
volume controlled HTA compared non-controlled. Resumed of 9 clinical
researches on the changing of GFR in HTA patients: CKD patient non-
controlled HTA (more than 140/90mmHg) – GFR decreased 12ml/min/year.
Inversing well control HTA (<130/80mmHg) GFR decreased 2ml/min/year.
(similar normal subject).
Peterson and al conclude RI and PI of renal arteries have closed
relationship with another HI and GFR.
In Vietnam, Tran Bui (2002) evaluated HI of renal arteries by Doppler
ultrasound. 35 normal subject competed 35 hypertensive’s patients with age
30-79. Blood follow (BF) in subject is 842ml/min. (HTA) (decreased
significality patients 262ml/min =24%.
Huynh Van Nhuan 2005 studied on 36 CKD compared 22 normal
showed RI and PI increased significality (0,79 compared 0,665) 2,13
compared 1,22.
Chapter 2
SUBJECT AND METHOD

2.1. Subject:
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- 333 peoples divide 2 groups: 136 normal and 197 HTA patients with age
40-90; among them 91 male and 106 female.
- Patients followed up in E hospital with essential HTA diagnosed,
proteinuria negative, GFR > 60ml/min.
2.2 Method:
- Perspective, controlled, description.
- Time of study: Jan/09 – Jan/2012
- Location: E hospital
2.2.2 Steps of study
Step 1: Chose study subject
Clinical consultation; BP measured, urin test 10 index, ultrasound kidney
and urology system.
Step 2:
- Measured BP; GFR test, MAU test, ultrasound Doppler kidney arteries.
- Collect research parameters recorded, and stopped all of HTA treatments
possible
Step 3: Analyze parameters collected by mathematical statistic SPSS 10.0
- Mean, SD
- Relationship under
- Compare mean, %
- Result statistical signification with p<0,05
- Result presented schema, table, image
Chapter 3
RESULT OF RESEARCH
3.1 Character of subjects
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Table 3.1: Mean age
Gender
Age (
X
± SD) (year)
p
HTA (n = 197) Control (n = 136)
Male (n=165) 59,1 ± 10,2 60,6 ± 9,7 >0,05
Female (n=168) 59,3 ± 9,3 59,3 ± 9,5 >0,05
p >0,05 >0,05
all 59,2 ± 9,7 60,0 ± 9,6 >0,05
Comment: mean age of HTA patients isn’t different normal subject with
p≥0,05 the same for gender
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Table 3.2. Stage of HTA
Age stage I n (%) Stage II n (%) p all n (%)
40-50 38 (88,4) 5 (10,6) < 0,05 43 (21,8)
51-60 35 (63,6) 20 (36,4) < 0,05 55 (27,9)
61-70 16 (25,8) 46 (74,2) < 0,05 62 (31,5)
> 70 2 (5,4) 35 (94,6) < 0,05 37 (18,8)
All 91(46,2) 106(53,8) < 0,05 197 (100)
Comment: percentage of HTA stage I higher than stage II sihnificaltly. No one
stageIII
3.2. Plasma concentration of renin (mg/l)
Table 3.3: PCR (mg/l)by age
Age
Renin (
X
± SD) (mg/l)

p
HTA(n=197) Control (n=136)
40-50(n=43) 2,70± 0,86 1,16 ± 0,11 < 0,05
51-60(n=55) 2,29 ± 0,71 1,27 ± 0,17 < 0,05
61-70(n=62) 2,24 ± 0,54 1,26 ± 0,17 < 0,05
>70(n=37) 1,75 ± 0,40 1,27 ± 0,17 < 0,05
all 2,26 ± 0,72 1,25 ± 0,16 < 0,05
p < 0,05 >0,05
Comment: PRC mean in HTA group higher than normal significaltly p<0,05.
More young more different in normal group PRC don’t change with age but in
HTA group PRC decreased with age.
Table 3.4: Percentage increased-decreased PRC
Age Increased
( >1,57 mg/l) n
Normal
(0,93 - 1,57mg/l) n
Decreased
(<0,93 mg/l) n (%)
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(%) (%)
40-50(n=43) 34 (23,6) 9 (17,0) 0
51-60(n=55) 39 (27,1) 16(30,2) 0
61-70(n=62) 48 (33,3) 14 (26,4) 0
>70(n=37) 23 (16,0) 14 (26,4) 0
All 144 (73,1) 53 26,9) 0
Comment: We defined normal range level of PRC 0,93-1,57 from table3.6. In
research 144 HTA PRC increased 73,1% and no one decreased different
significantly.
3.3. Microalbuminuria

Table 3.5: Microalbuminuria
Gender
Microalbuminuria
MAU (+) n (%) Concentration (mg/24h) (
X
± SD)
Male (n=91) 32 (56,1) 43,9 ± 64,3
Female (n=106) 25 (43,9) 31,5 ± 60,9
p < 0,05 >0,05
All (n=197) 57 (28,9) 37,9 ± 62,9
Comment: 57 patients with microalbuminuria (+) is 28,9%. among microalbumin
(+), male 56,1% female is 43,9%, diferent significalty p<0,05.
Table 3.6: microalbuminuria by time of HTA
Time (year) Microalbumin (+)
n (%)
Microalbumin (-)
n (%)
<1 (n=39) 5 (8,8) 13 (9,3)
1-5 (n=67) 34 (59,6) 109 (77,8)
>5 (n=91) 18 (31,6) 18 (12,9)
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p <0,05 <0,05
All 57 (28,9) 140 (71,1)
Comment: microalbumin (+) increased by time and diferent significalty p<0,05
compared microalbumin negative.
Table 3.7: microalbuminuria by stage of HTA
Stage Microalbumin (+) n
(%)
Microalbumin (-) n

(%)
p
I (n=91) 13 (22,8) 78 (55,7) <0,05
II (n=106) 44 (77,2) 62 (44,3) <0,05
p <0,05 >0,05
OR 4,258
Comment: Microalbuminuria (+) increased by stage HTA significalty p<0,05.
Patients HTA stage II risk microalbumin niệu (+) higher 4,258 time stage I. diferent
significalty p<0,05 microalbumin (+) and microalbumin niệu (-) by stage.
3.4. Gromerular filtration rate (GFR)
Table 3.8: GFR (ml/min) by age
Age
GFR (
X
± SD ) (ml/min)
p
HTA (n=197) Control (n=136)
40-50(1)
(nb=43)(nc=20)
86,3 ± 8,5 103,9 ± 11,0 <0,05
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51-60(2)
(nb=55)(nc=42)
81,6 ± 9,3 95,7 ± 10,2 <0,05
61-70(3)
(nb=62)(nc=44)
72,4 ± 6,3 85,3 ± 8,6 <0,05
> 70(4)
(nb=37)(nc=30)

73,2 ± 6,5 82,4 ± 9,1 <0,05
All
(nb=197)(nc=136)
78,2 ± 8,8 90,6 ± 9,5 <0,05
p p¹ p² <0,05 p¹ p²<0,05
(pº: p2/1; p¹: p3/1; p²: p4/1; p³: p4/2) (nb: HTA; nc: Control).
Comment: GFR decreased by age in two group significalty.
Table 3.9: GFR (ml/min) by HTA stage
Age
GFR (
X
± SD ) (ml/min)
p
stage I (n=91) stage II (n=106)
40-50 (n=43) 87,5 ± 8,7 86,6 ± 7,2 >0,05
51-60 (n=55) 80,7 ± 9,3 83,1 ± 9,3 >0,05
61-70 (n=62) 77,1± 7,5 75,3± 7,1 >0,05
> 70 (n=37) 76,2 ± 7,9 73,0 ± 6,3 >0,05
All (n=197) 81,1 ± 8,6 75,6 ± 7,9 <0,05
Comment: GFR diferent significalty p<0,05 betwen stage I and II.
Table 3.10: GFR (ml/min) by time of HTA
Time (year)
GFR (
X
± SD ) (ml/min)
<1 (n=39) 71,5 ± 23,9
1-5 (n=67) 78,1 ± 19,3
>5 (n=91) 81,8 ± 18,9
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All (n=197) 78,2 ± 8,8
p > 0,05
Comment: by time HTA, GFR seem decreased but not significalty.
3.5. Hemodynamic index of kidney arteries
Table 3.11: Blood flow volume (ml/min) right and left by age
Age
BFV (
X
± SD) (ml/min)
Right Left p all
40-50 HTA 476,6 ± 88,9 505,1 ± 82,1 >0,05 981,6 ± 170,2
Control 597,6 ± 64,3 605,9 ± 63,8 >0,05 1203,5 ± 127,7
p <0,05 <0,05 <0,05
51-60 HTA 443,8 ± 66,0 473,2± 67,7 >0,05 909,8 ± 139,9
Control 546,1 ± 94,1 556,2 ± 89,1 >0,05 1102,3 ± 182,8
p <0,05 <0,05 <0,05
61-70 HTA 429,7 ± 20,0 461,2 ± 26,4 >0,05 890,9 ± 42,9
Control 500,9 ± 151,2 502,6 ± 150,9 >0,05 1003,5 ± 301,6
p <0,05 >0,05 <0,05
> 70 HTA 434,6 ± 13,0 459,2 ± 21,1 >0,05 893,8 ± 29,7
Control 454,2 ± 147,4 461,9 ± 146,9 >0,05 916,1 ± 293,8
p >0,05 >0,05 >0,05
All HTA 444,8 ± 58,0 473,7 ± 57,5 >0,05 916,5 ± 116,6
Control 518,8 ± 131,9 525,4 ± 131,2 >0,05 1044,2 ± 262,6
p <0,05 <0,05 <0,05
Comment: BFV no different betwen kidney right and left.
Table 3.12: BFV by time HTA
Age
BFV (
X

± SD) (ml/min)
Stgae I (n=91) Stage II (n=106) p All
40-50 (1)
(n=43)
990,3 ± 179,3 915,7 ± 27,8 <0,05
981,6 ±
170,2
51-60 (2) 922,6 ± 172,5 887,3 ± 39,7 <0,05 909,8 ±
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(n=55) 139,9
61-70 (3)
(n=62)
898,7 ± 27,1 888,2 ± 47,1 >0,05 890,9 ± 42,9
> 70 (4)(n=37) 880,7 ± 39,9 894,5 ± 29,6 >0,05 893,8 ± 29,7
All (n=197) 945,8 ± 161,6 891,4 ± 39,9 <0,05
916,5 ±
116,6
Comment: BFV in HTA sage II lower than HTA stage I significalty.
Table 3.13: Speed of blood flow (cm/s) by position
Index Entry of artery Hile Parenchyme p
Vs (
X
± SD) (cm/s)
98,0 ± 7,2 51,7 ± 6,0 32,3 ± 4,9 <0,05
Vd (
X
± SD) (cm/s)
33,9 ± 4,9 22,3 ± 4,9 13,5 ± 4,7 <0,05
Vm (

X
± SD) (cm/s)
50,8 ± 5,0 35,3 ± 4,9 20,4 ± 4,9 <0,05
Comment: BF different in 3 position, decreased from out to centre.
Table 3.14: RI, PI
Index Entry of artery Hile Parenchyme
RI
(
X
± SD)
Right 0,63 ± 0,08 0,59 ± 0,08 0,59 ± 0,09
Left 0,64 ± 0,08 0,62 ± 0,09 0,59 ± 0,09
All 0,63 ± 0,06 0,61 ± 0,07 0,59 ± 0,08
Right 1,00 ± 0,15 0,92 ± 0,18 0,98 ± 0,18
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PI
(
X
± SD)
Left 1,04 ± 0,18 0,95 ± 0,12 0,97 ± 0,15
All 1,02 ± 0,14 0,94 ± 0,11 0,97 ± 0,14
Comment: RI , PI decreased from outside to parenchym. No different betwen right
and left.
3.6. Relationship of BFV, GFR, PCR
3.6.1. Parameters of entry position
Table 3.15: BFV (ml/min) by microalbuminuria
Age
BFV (
X

± SD) (ml/phút)
p
Mcroalbumin (+)
(n=57)
Microalbumin (-)
(n=140)
40-50 (n=43) 895,5 ± 11,8 990,5 ± 176,5 >0,05
51-60 (n=55) 866,3 ± 54,7 919,4 ± 151,3 >0,05
61-70 (n=62) 885,6 ± 57,2 895,6 ± 24,3 >0,05
> 70 (n=37) 895,6 ± 33,9 892,7 ± 27,6 >0,05
All (n=197) 885,4 ± 49,9 929,2 ± 132,6 >0,05
Comment: In group microalbuminuria (+) BFV seem decreased compared group
microalbumin (-) but not significalty.
Table 3.16. Relationship of BFV with speed flow and artery surface
Parameters
Right Left
HTA control HTA control
Vm (cm/s) 53,3 53,3 48,3 48,7
BFV (ml/min) 444,8 518,8 473,7 525,4
Surface (cm2) 0,14 0,16 0,16 0,18
Comment: BFV and surface of kidnet arteries decreased in group HTA significalty but not
Vm.
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Table 3.17: Relationship of BFV with another parameters
Parameters r p
GFR 0,279 (Pearson) <0,05
Renin (PCR) 0,076 (Spearman) 0,290
RI -0,136 (Pearson) <0,05
PI -0,150 (Pearson) <0.05

Mean blood pressure -0,126 (Spearman) 0,078
Comment: BFV had relationship with GFR (r = 0,279 và p<0,05) and RI, PI but not
with PCR.
3.6.2. GFR Correlation with another parameters
Bảng 3.18: GFR (ml/min) by Microalbuminuria
Stage HTA
GFR (
X
± SD) (ml/min)
p
Microalbumin (+)
(n=57)
Microalbumin (-)
(n=140)
I (n=91) 78,8 ± 8,0 81,5 ± 9,3 >0,05
II (n=106) 73,1 ± 6,8 77,4 ± 8,1 >0,05
All (n=197) 74,4 ± 7,1 79,7 ± 8,5 >0,05
p >0,05 >0,05
Comment: GFR in microalbumin (+) lower than group (-) but not significalty
p>0,05.
Bảng 3.19: Correlation of GFR with another parameters
Parameters r p
BP systolic -0,096 (Pearson) 0,177
PCR 0,033(Spearman) 0,643
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Vm 0,174 (Pearson) 0,014
RI -0,300 (Pearson) <0,001
PI -0,127 (Pearson) 0,076
Comment: GFR had no collerated with BPS, PCR, PI but collerated with Vm and RI.

3.6.3. Correlation of RI and PI
Bảng 3.20: RI, PI by microalbuminuria
RI-PI
Microalbumin (+)
(n=57)
Microalbumin (-)
(n=140)
p
Entry
RI (
X
± SD)
0,66 ± 0,08 0,61 ± 0,07
<0,05
PI (
X
± SD)
1,02 ± 0,19 0,99 ± 0,13
>0,05
Hile
RI (
X
± SD)
0,60 ± 0,09 0,59 ± 0,07
>0,05
PI (
X
± SD)
0,89 ± 0,18 0,94 ± 0,18
>0,05

Parenchy
m
RI (
X
± SD)
0,60 ±0,08 0,58 ±0,09
>0,05
PI (
X
± SD)
1,01 ±0,22 0,97 ±0,16
>0,05
Comment: group microalbumin (+) have RI, PI no different with microalbumin (-).
Table 3.21: Correlation of RI, PI with BP and PCR
RI PI
r p r p
Mean BP -0,032 0,652 0,072 0,317
BP systolic 0,096 0,179 0,059 0,410
BP diastolic -0,039 0,586 0,056 0,433
Renin PCR -0,168 0,019 -0,018 0,797
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Comment: RI , PI had no related with BP and PCR
Chapter 4.
DISCUSSION
4.1. Characteristics of age
Our study shows that hypertension increases with age: under 50 years group was
21.8%, the age group 50-60 is 27.9%, the group of 61-70 years was 31.5%; 70-year-
old group was 18.8%. The results of our study are similar to the study by Pham Thi
Kim Lan (2002), Dong Van Thanh (2011). According to the JNC VII, hypertensive

kidney disease increases with age. Most cases are diagnosed with kidney disease are
hypertension, the middle-aged and elderly people. These groups are very difficult to
distinguish the vascular damage due to age or due to hypertension.
4.2. Blood pressure
Analysis by stage of hypertension we found: There are 91 patients with stage I
accounted for 46.2%. 106 patients with stage II, 53.8%. The difference in this
proportion significantly p <0.05. Most patients with hypertension in this study was
mild to moderate. In this study, no patients with stage III hypertension. According to
the classification of hypertension by the world health organization, hypertensive
patients with stage III when there are more than 2 target organ damage. Meanwhile,
the agency is soon hurt the eyes and kidneys. When excluding patients with
proteinuria were broadly positive, the patient did not see any blood pressure over 2
organ damage.
4.3. Change the concentration of blood rennin
Important mechanism between renal damage and hypertension role of
aldosterone-renin-angiotensin system. We examined blood parameters renin to learn
this association. In the present study we found that the concentration of renin in
hypertension 197 (2.26 mg / l) significantly greater than the concentration of renin in
136 people in the control group (1,25mg / l). In the subgroup of patients renin
concentration decreases with age have statistically significant p <0.05. While in the
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control group relative renin concentration constant. Thus the concentration in the
blood renin hypertension decreased with age, while those without hypertension renin
levels stable. Fink H.A. 2012 study of renal lesions seen in patients with chronic
kidney disease, the angiotensin converting enzyme inhibitors and AT1 receptor
inhibition reduces the risk of end-stage renal failure, reduced mortality risk of
myocardial infarction and sudden stroke, thereby confirming the role of the renin-
angiotensin system-aldosterone in target organ damage in hypertensive patients.
4.4. Change in glomerular filtration rate

Glomerular filtration rate decreases with increasing blood pressure stage. This
may indicate that the glomerular filtration rate depends on the internal blood
pressure and glomerular affected by systemic blood pressure, higher blood pressure,
increased glomerular filtration rate decreases. Initial blood pressure makes the blood
flow to the kidneys increases and increased glomerular filtration rate. But then over
time the response of the kidney is no longer as in the first phase and to a certain time
point, the glomerular filtration rate will decrease rather than increase. Through
research can see clearly the relative influence of blood pressure on glomerular
filtration rate.
Author Puttinger H. 2003 study in Austria found that hypertensive renal disease
is the main cause of end-stage renal failure. When kidney function is severely
impaired control of blood pressure treatment and maintain kidney function very
difficult. This study shows that the achieved blood pressure control targets to reduce
CKD patients as well as blocking lesions in other organ.
Table 4.1. Change glomerular filtration rate in patients with hypertension.
Author GFR(ml/min/1,73m2)
We 78,2
I-SEARCH Việt Nam 65,8
I-SEARCH global 87,9
London G.M. 73
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Farbom P. 89,1
Pontromeli 87
4.5. Change renal blood flow
In people with primary hypertension renal blood flow is 916,5ml / min in
healthy blood flow to the kidneys is 1044.2 ml / min. The difference between the two
groups is statistically significant. When hypertensive renal blood flow will decrease,
reducing the operational capability of the kidneys and renal nutrition. External
causes pressure problems are caused by progressive renal fibrosis in patients with

hypertension in a long time. Analysis by age and stage of hypertension and saw the
blood flow to the kidneys in people with stage I hypertension greater than those with
hypertension stage II. This can be explained in the early stages when the kidneys are
not damaged, more fibrosis, renal blood flow depends mainly on the blood pressure
high blood pressure, the blood flow to the kidney. Over time as renal lesions of the
renal response to blood pressure numbers are not as original and renal blood flow are
not dependent on blood pressure numbers more
Table 4.2. Renal blood flow (ml/min) in patients with hypertension
Author BFV Reduction%
We 916,5 12,2
Trần Bùi 842 24
London GM 739 17,1
Author Gomez-marcos M.A. 2012 Spanish study of 258 patients with
hypertension found that renal blood flow correlated inversely with glomerular
filtration rate. This author also hypothesized about the role of inflammatory factors
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with the elasticity of blood vessels in understanding inflammatory factors CRPHS
sensitive to elasticity.
4.6. Impedance change index (RI) and pulse index (PI)
Research on the index and renal vascular resistance index of renal artery RI dam,
PI found no differences were statistically significant between RI and PI indices in the
right kidney and left kidney, between the disease and the control group. We analyze
the impedance index RI phased hypertension and found that RI and PI increased in
phases hypertension. Our analysis of the RI index according to renal damage through
microalbuminuria is a sign that there is no significant difference between the two
groups. Thus the resistance index increased significantly when measured at early
manifestations of kidney parenchyma. While expression as measured in umbilical
artery and kidney of unknown origin by. Cao Xuan Cuong 2011 study of patients
with diabetes and Tran Thi Bach Tuyet authors monitored 2008 patients with renal

impairment results in higher PI and RI of us. Perhaps kidney damage due to
hypertension early period no changes to the parameters of the PI RI clearly on
ultrasound as patients with diabetes or renal insufficiency. Author DEEG K.H. 2003
Dopple ultrasound study in 147 renal artery. Authors found different in the original
RI renal artery, umbilical kidney and renal parenchyma. RI at the base of the renal
artery was 0.69 ± 0.09; 0.63 ± 0.08 hilus and 0.60 ± 0.16 in the renal parenchyma. RI
increases with age.
4.7. Related renal blood flow and blood pressure
Our research indicates differences statistically significant decline in renal blood
flow in hypertension stage I and II show the effects of hypertension on renal blood
flow. In the present study, we found that in those with positive microalbuminuria and
nephropathy that is clearly renal blood flow was 885.4 ml / min lower than that of
those with hypertension microalbuminuria negative is 929,2ml / min. Interaction
between the blood flow through the kidneys and hypertension is a vicious cycle.
Reduced flow will induce hypertension, but the long-term pressure due to
hypertension disrupts the normal structure and whether the traffic has increased, the
ability of the kidneys filter is not improved. Reduced blood flow in the ischemic
kidney causing kidney tissue nourished fibrosis leading to renal parenchyma.
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Patients with prolonged hypertension, increased peripheral resistance, aortic elastic
properties of large arteries and reduce the damage caused by the arterial wall. Wall of
the aorta and large arteries dilated opposed to the peripheral arteries. Key to this
transformation renal parenchymal damage, kidney damage until fibrosis, renal
parenchymal area decreased, blood vessels constrict or fibrous tissue surrounding
pinched, pull, so the blood flow in the kidney reduced.
4.8. Related renal blood flow and glomerular filtration rate
In our research shows that there is a correlation between renal blood flow and
glomerular filtration rate with r = .279, this correlation was statistically significant
with p <0.05. Author DEEG K.H. 2003 study renal artery Doppler ultrasonography

in 147 people found renal blood flow in the body different renal artery, umbilical
kidney and renal parenchyma. Flow from the lower umbilical artery 30% of the
body; parenchyma 30% lower than the navel and clearly related to renal clearance.
Martynov S A author. in 2003 assess renal artery blood by ultrasound. The survey
found 50 patients with renal perfusion is reduced by 36%. Concentration of
creatinine, glomerular filtration rate correlated with renal blood flow measured at the
hole in the parenchyma and in. Patients with higher age of increasing RI.
Table 4.3. Correlation between renal blood flow and glomerular filtration rate
Author Correlation coefficient (r)
we 0,279
Makino Y. 0,56
Lebkowka U. 0,38
4.9. Related glomerular filtration rate and hypertension
In the early stages of hypertension increased glomerular vascular pressure
response to blood pressure puts increased glomerular filtration rate in early stage and
mild. In contrast to the blood pressure in people with hypertension stage II, the
inverse correlation between blood pressure and glomerular filtration rate is a lot
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clearer. We thought at the time was new hypertension or hypertension and mild early
stage, the glomerular filtration rate seems to increase with events, but then the
response time with the number of glomerular hypertension unlike previous stage
filtration rate of the kidneys which will decrease the high blood pressure. We see
more clearly in the two groups of hypertension stage I and stage II hypertension and
found that glomerular filtration rate correlated with urinary microalbumine
hypertensive group did not close the first phase of the relationship between the
glomerular filtration with microalbuminuria in hypertensive group phase II.
Statistical significance of the correlation between glomerular filtration rate and
microalbuminuria in hypertensive group, Phase I, while the statistical significance of
the correlation between glomerular filtration rate and urinary microalbumine

hypertension in group stage II above.
According to the KDOQI 2002 hypertensive group stages II and III have the
speed reduced glomerular filtration rate and always goes down very fast, whereas the
group with hypertension stage I early glomerular filtration rate increased slightly and
then decreases with time. Hypertension is a major cause of disease on cardiovascular
events and kidney damage. Lash and his colleagues in 2009 CRIC study results
confirmed the correlation between kidney function and risk factors such as
hypertension, obesity.
4.10. Related glomerular filtration rate and blood flow velocity index renal
vascular resistance RI, PI index pulse
When considering the interrelationships of glomerular filtration rate with a
hemodynamic parameters and found a negative correlation are relatively unknown.
For the average blood flow velocity V must be careful correlation of r = 0.174
moderate, p = 0.014, with resistance index RI right kidney, the correlation coefficient
was r = -0.3, the correlation has statistically significant with p <.001. Glomerular
filtration rate correlated well with the PI index of the right kidney with a correlation
coefficient r = -0.127, this correlation was not statistically significant with p = 0.076.
Table 4.4. Correlation between glomerular filtration rate and resistance index RI
Author Correlation coefficient (r)
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We -0,3
Makino -0,39
Galesic K -0,383
Vigna -0,59
Petersen LJ -0,5
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CONCLUSION
Studied 197 patients with primary hypertension, proteinuria broadly negative

and 136 normal people of the same age are doing renal artery Doppler
ultrasonography and measurement of glomerular filtration rate, we draw some
conclusions follows:
1. Regarding the hemodynamic parameters and renal artery glomerular
filtration rate in patients with primary hypertension
- Renal blood flow velocity (Vs, Vd, Vm) decreases from umbilical cord stem
renal artery to the kidney and the renal parenchyma. Microalbuminuria group (+)
parameters lower than microalbuminuria group (-).
- 2 renal blood flow measurements in the renal artery origin tends to decrease
with age (40-50 years of age: 981.6 ± 170,2ml / min, over 70 years of age: 893.8 ±
29,7ml / min ), the lower the disease control group (916.5 ± 116,6ml / min and
1044.2 ± 262,6ml / min), decreased with increasing blood pressure stage (stage I:
945.8 ± 161,6ml / ph, phase II: 891.4 ± 39,9ml / min). Renal blood flow in group
MAU (+) group had lower MAU (-) (885.4 ± 49,9ml / min versus 929.2 ± 132.6
mL / min).
- The average value of RI and PI tends to increase with age and according to the
stage of hypertension. Group MAU (+) with higher RI and PI blood group (-): RI =
0.66 ± 0.08 versus 0.61 ± 0.07; PI = 1.02 ± 0.19 versus 0.99 ± 0.13.
- Glomerular filtration rate tends to decrease with age (40-50 years: 86.3 ml /
min / 1,73m2; over 70: 73.2 ml / min / 1,73m2; decreases blood stage pressure (stage
I: 81.1 ml / min / 1,73m2, stage II: 75.6 ml / min / 1,73m2), decreasing over time to
detect hypertension (less than 1 year: 71.5 ml / min / 1,73m2, in 5 years: 81.8 ml /
min / 1,73m2). group MAU (+) had lower glomerular filtration rate MAU group (-)
(74.4 ml / min / 1 , 73m2 compared with 79.7 ml / min / 1,73m2).
- The average concentration of renin in the blood is higher than the control group
patients (2.26 ± 0,72mg / l versus 1.25 ± 0,16mg / l). In the control group blood
renin levels do not change with age. In the subgroup of patients with plasma renin
concentration by age (40-50 years old: 2.70 ± 0.86 mg / l compared to 70 years: 1.75
± 0.40 mg / l).
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2. The relation of renal blood flow, glomerular filtration rate with renin and
blood parameters of renal artery hemodynamics
- Renal blood flow was inversely correlated with the RI, PI in the renal
parenchyma (r = -0.136, p <0.05; r = -0.15, p = 0.036), correlated with the
glomerular filtration rate (r = 0.279, p <0.05).
- Glomerular filtration rate was inversely correlated with RI (r = - 0.30, p
<0.001); correlated with systolic blood flow velocity V (r = 0.174, p = 0.014).
- The right kidney RI inversely correlated with blood plasma renin concentration
(r = - 0.168, p = 0.019).
RECOMMENDATIONS
The study results contribute to confirm the change of parameters of renal
hemodynamics and glomerular filtration rate in relation to the status of hypertension
in patients with primary hypertension in hypertensive phase, time disease and
severity of kidney damage. On the basis of the results obtained recommends
clinicians a comprehensive assessment, systematic, periodic parameters of renal
artery hemodynamics, glomerular filtration rate, blood renin levels to detect injuries
kidney damage caused by hypertension.
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