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

  • Số trang: 28 |
  • Loại file: DOCX |
  • Lượt xem: 17 |
  • Lượt tải: 0
nhattuvisu

Đã đăng 26946 tài liệu

Mô tả:

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 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 Find thesis in 1. National library 2. Vietnam military medical university year 2014 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 2nd 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 - 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 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 noncontrolled 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: - 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 Table 3.1: Mean age Gender Male (n=165) Age ( X ± SD) (year) HTA (n = 197) Control (n = 136) 59,1 ± 10,2 60,6 ± 9,7 p >0,05 Female (n=168) 59,3 ± 9,3 59,3 ± 9,5 p >0,05 >0,05 all 59,2 ± 9,7 60,0 ± 9,6 >0,05 >0,05 Comment: mean age of HTA patients isn’t different normal subject with p≥0,05 the same for gender 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 Normal ( >1,57 mg/l) n (0,93 - 1,57mg/l) n (%) 34 (23,6) 39 (27,1) 48 (33,3) 23 (16,0) 144 (73,1) 40-50(n=43) 51-60(n=55) 61-70(n=62) >70(n=37) All Decreased (%) 9 (17,0) 16(30,2) 14 (26,4) 14 (26,4) 53 26,9) (<0,93 mg/l) n (%) 0 0 0 0 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 Microalbuminuria Gender 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) <1 (n=39) Microalbumin (+) Microalbumin (-) n (%) n (%) 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) 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 (%) (%) 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 p 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 ( HTA (n=197) X ± SD ) (ml/min) Control (n=136) p 40-50(1) (nb=43)(nc=20) 51-60(2) (nb=55)(nc=42) 61-70(3) (nb=62)(nc=44) > 70(4) (nb=37)(nc=30) All (nb=197)(nc=136) p 86,3 ± 8,5 103,9 ± 11,0 <0,05 81,6 ± 9,3 95,7 ± 10,2 <0,05 72,4 ± 6,3 85,3 ± 8,6 <0,05 73,2 ± 6,5 82,4 ± 9,1 <0,05 78,2 ± 8,8 90,6 ± 9,5 <0,05 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 X GFR ( ± SD ) (ml/min) stage I (n=91) stage II (n=106) 87,5 ± 8,7 86,6 ± 7,2 80,7 ± 9,3 83,1 ± 9,3 77,1± 7,5 75,3± 7,1 76,2 ± 7,9 73,0 ± 6,3 81,1 ± 8,6 75,6 ± 7,9 Age 40-50 (n=43) 51-60 (n=55) 61-70 (n=62) > 70 (n=37) All (n=197) p >0,05 >0,05 >0,05 >0,05 <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) <1 (n=39) GFR ( X ± SD ) (ml/min) 71,5 ± 23,9 1-5 (n=67) 78,1 ± 19,3 >5 (n=91) 81,8 ± 18,9 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 40-50 51-60 61-70 > 70 All BFV ( X ± SD) (ml/min) Right Left p all 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 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 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 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 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 Comment: BFV no different betwen kidney right and left. <0,05 <0,05 <0,05 >0,05 <0,05 Table 3.12: BFV by time HTA BFV ( Age X ± SD) (ml/min) Stgae I (n=91) Stage II (n=106) p 990,3 ± 179,3 915,7 ± 27,8 <0,05 922,6 ± 172,5 887,3 ± 39,7 <0,05 898,7 ± 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 40-50 (1) (n=43) 51-60 (2) (n=55) 61-70 (3) (n=62) All 981,6 ± 170,2 909,8 ± 139,9 916,5 ± 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 Vs ( Vd ( Vm ( X X X ± SD) (cm/s) ± SD) (cm/s) ± SD) (cm/s) Entry of artery Hile Parenchyme p 98,0 ± 7,2 51,7 ± 6,0 32,3 ± 4,9 <0,05 33,9 ± 4,9 22,3 ± 4,9 13,5 ± 4,7 <0,05 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 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 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 RI ( X ± SD) PI ( X ± SD) 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 BFV ( Age X ± SD) (ml/phút) p Mcroalbumin (+) Microalbumin (-) (n=57) (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 Right Left Parameters 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. Table 3.17: Relationship of BFV with another parameters Parameters GFR Renin (PCR) RI PI Mean blood pressure r 0,279 (Pearson) 0,076 (Spearman) -0,136 (Pearson) -0,150 (Pearson) -0,126 (Spearman) p <0,05 0,290 <0,05 <0.05 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 GFR ( Stage HTA X ± SD) (ml/min) p Microalbumin (+) Microalbumin (-) (n=57) (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 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 Entry RI ( PI ( Hile RI ( PI ( Parenchy m RI ( PI ( X X X X X X ± SD) ± SD) ± SD) ± SD) ± SD) ± SD) Microalbumin (+) Microalbumin (-) (n=57) (n=140) 0,66 ± 0,08 0,61 ± 0,07 1,02 ± 0,19 0,99 ± 0,13 0,60 ± 0,09 0,59 ± 0,07 0,89 ± 0,18 0,94 ± 0,18 0,60 ±0,08 0,58 ±0,09 1,01 ±0,22 0,97 ±0,16 p <0,05 >0,05 >0,05 >0,05 >0,05 >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 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-yearold 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 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 reninangiotensin 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
- Xem thêm -