hypertensive kidney injury and the progression of … kidney injury and the progression of chronic...
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![Page 1: Hypertensive Kidney Injury and the Progression of … Kidney Injury and the Progression of Chronic Kidney Disease Karen A. Griffin, M.D. Professor of Medicine Loyola University Medical](https://reader030.vdocuments.us/reader030/viewer/2022011802/5b09880b7f8b9a5f6d8e10e2/html5/thumbnails/1.jpg)
Hypertensive Kidney Injury and the Progression of Chronic Kidney Disease
Karen A. Griffin, M.D.Professor of Medicine
Loyola University Medical CenterRenal Section Chief
Edward Hines, Jr. V.A. Hospital
![Page 2: Hypertensive Kidney Injury and the Progression of … Kidney Injury and the Progression of Chronic Kidney Disease Karen A. Griffin, M.D. Professor of Medicine Loyola University Medical](https://reader030.vdocuments.us/reader030/viewer/2022011802/5b09880b7f8b9a5f6d8e10e2/html5/thumbnails/2.jpg)
Hypertension in the United States75 million
< 0.5% ESRD
USRDS Annual Report
![Page 3: Hypertensive Kidney Injury and the Progression of … Kidney Injury and the Progression of Chronic Kidney Disease Karen A. Griffin, M.D. Professor of Medicine Loyola University Medical](https://reader030.vdocuments.us/reader030/viewer/2022011802/5b09880b7f8b9a5f6d8e10e2/html5/thumbnails/3.jpg)
Susceptibility Patterns of Hypertensive Renal Damage
100 140 180 220 260
Systolic Blood Pressure (mmHg)
Rena
l Dam
age Malignant
NephrosclerosisDiabetic Nephropathy / Chronic Kidney DiseaseAccelerated GS
Benign Nephrosclerosis
Bidani and Griffin , Hypertension 2004; 44: 595-601
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Loutzenhiser, Griffin, Williamson, Bidani Am J Physiol 2006; 90:R1153-R1167(Griffin et al, Am J Hypertens 2001;14:311-320; Bidani et al, Am J Physiol 1993;265:F391-398
r2=0.77 r2=0.59
Hypertensive Renal DamageSusceptibility Patterns in Experimental Models
100 140 180 220 260Average Systolic BP, mmHg
0
25
50
Ren
al D
amag
e Sc
ore
SHRsp (n=10)SHRsp + NaCl (n=18)
SHR (n=9)SHR + NaCl (n=16)
RK-I (n=16)
Sprague-DawleyControl (n=7)
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Remnant Kidney Model of CKD(5/6 Ablation)
• Compensatory Hyperfiltration and Hypertrophy
• Hypertension
• Proteinuria
• Progressive GS
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Loutzenhiser, Griffin, Williamson, Bidani Am J Physiol 2006; 90:R1153-R1167Griffin et al, Am J Hypertens 2001;14:311-320; Bidani et al, Am J Physiol 1993;265:F391-398
r2=0.77 r2=0.59
Hypertensive Renal DamageSusceptibility Patterns in Experimental Models
100 140 180 220 260Average Systolic BP, mmHg
0
25
50
Ren
al D
amag
e Sc
ore
SHRsp (n=10)SHRsp + NaCl (n=18)
SHR (n=9)SHR + NaCl (n=16)
RK-I (n=16)
Sprague-DawleyControl (n=7)
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Vasodilation
Bidani et al. AJP 252: F1003-F1010, 1987; Griffin et al, JCI 96: 793-800, 1995; Griffin et al, KI 55: 1849-1860, 1999; Bidani et al. AJP 285: F113-F120, 2003
Renal Autoregulation and Susceptibility to Hypertensive Damage
Rena
l Blo
od F
low
(%)
Arterial Pressure, mmHg
50
100
150
200
60 90 120 150 180 210 240
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Susceptibility Patterns of Hypertensive Renal Damage
100 140 180 220 260
Systolic Blood Pressure (mmHg)
Rena
l Dam
age Malignant
NephrosclerosisDiabetic Nephropathy / Chronic Kidney DiseaseAccelerated GS
Benign Nephrosclerosis
Bidani and Griffin , Hypertension 2004; 44: 595-601
![Page 9: Hypertensive Kidney Injury and the Progression of … Kidney Injury and the Progression of Chronic Kidney Disease Karen A. Griffin, M.D. Professor of Medicine Loyola University Medical](https://reader030.vdocuments.us/reader030/viewer/2022011802/5b09880b7f8b9a5f6d8e10e2/html5/thumbnails/9.jpg)
SHRsp Model of Malignant Nephrosclerosis(Prevention)
Griffin KA et al., Hypertension 2014;64:801-7
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SHRsp Model of Malignant Nephrosclerosis(Prevention)
Griffin KA et al., Hypertension 2014;64:801-7
Ren
al D
amag
e Sc
ore
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SHRsp Model of Malignant Nephrosclerosis(Repair)
Griffin KA, et al., Hypertension 2014;64:801-7
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SHRsp Model of Malignant Nephrosclerosis(Repair)
Griffin KA, et al., Hypertension 2014;64:801-7
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Remnant Kidney Model of CKD(5/6 Ablation)
• Compensatory Hyperfiltration and Hypertrophy
• Hypertension
• Proteinuria
• Progressive GS
Hyperfiltration vs. Hypertension
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Pathogenesis of Glomerulosclerosisin Renal Mass Reduction Models
Griffin et al, JASN 1994; 4: 2023-2031
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Griffin et al, JASN 1994; 4:2023-2031
Pathogenesis of Glomerulosclerosisin Renal Mass Reduction Models
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Griffin et al, JASN 1994; 4: 2023-2031
Pathogenesis of Glomerulosclerosisin Renal Mass Reduction Models
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• Normal Pregnancy (AJKD 1989; 290-298)• Renal Transplant Donors (NEJM 2009; 360:459-469)
Hyperfiltration in Normotensive States
Minimal glomerulosclerosis
QA, Kf (GC Volume)
Hypertensive States: PGC, but Kf due to a reciprocal relationshipAJP 1980; 239:F171-F186; AJP 1981; 240:F245-254; JCI 1986; 77:1993-2000
Bidani, et al. KI 1990; 38:28-38; Griffin, et al. JASN 1994; 4:2023-2031.
Griffin, et al. AJP 2008; 294:F685-F696
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SPONTANEOUSLY HYPERTENSIVE RAT RENAL ABLATION BY INFARCTION RENAL ABLATION BY EXCISIONAVE. SYST. BP: 214 mm Hg AVE. SYST. BP: 214 mm Hg AVE. SYST. BP: 133 mm Hg
INTACT AUTOREGULATION IMPAIRED AUTOREGULATION IMPAIRED AUTOREGULATIO
EFFECTS OF HYPERTENSION AND IMPAIRED AUTOREGULATION ON CKD PROGRESSION (8 WEEKS – Hematoxylin/Eosin)
Venkatachalam, et al., Am J Physiol. 2010; 298: 1078-1094
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Vasodilation
Bidani et al. AJP 252: F1003-F1010, 1987; Griffin et al, JCI 96: 793-800, 1995;Griffin et al, Am J Physiol Renal Physiol. 2004;286:F1136-43; Bidani et al. AJP 285: F113-F120, 2003
Renal Autoregulation and Susceptibility to Hypertensive Damage
Rena
l Blo
od F
low
(%)
Arterial Pressure, mmHg
50
100
150
200
60 90 120 150 180 210 240
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Griffin et al, JCI 1995; 96:793, KI 1999; 55: 1849, Hypertens 2001; 37: 1268,Bidani et al, Kidney Int 2000; 57: 1651
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0 2 5 5 0 7 5 1 0 0 1 2 5 1 5 080
120
160
200
Ave
rage
Sys
tolic
BP,
mm
Hg
0
10
20
30
40
HIR
D S
core
RK-I (n=16)
P <0.01 maximum vs RK-I
**
SHRsp (n=27)
Bidani et al, Am J Physiol 1993;265:F391-398; Griffin KA, et al., Hypertension 2014;64:801-7
Ren
al D
amag
e Sc
ore
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Bidani et al, Am J Physiol 1993;265:F391-398; Griffin KA, et al., Hypertension 2014;64:801-7;Polichnowski, et al. Am J Physiol 2015; 308:F252-F260
Ren
al D
amag
e Sc
ore
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100 125 150 175 200 225 250Average SBP, mmHg
0
25
50
75
Com
posi
te H
IRD
Sco
re
SHRsp (n=27)RK-I (n=16)
Angiotensin II (n=19)
Quantitative Relationship BetweenBP and Renal Injury
Bidani et al, Am J Physiol 1993;265:F391-398; Griffin KA, et al., Hypertension 2014;64:801-7;Polichnowski, et al. Am J Physiol 2015; 308:F252-F260
Ren
al D
amag
e Sc
ore
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Angiotensin II10 seconds
10 seconds
Polichnowski AJ et al: Am J Physiol 2013; 305:F1074-F1084
BP – RBF Relationships in Conscious Angiotensin II vs. Phenylephrine-induced Hypertensive Rats
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Susceptibility to Hypertensive Renal Damage
Efferent Arteriole
Glomerular CapillaryPressure (45-50 mmHg)
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NOS Expression in the Renal Microvasculature
nNOSeNOS
Bachmann, et al., Am J Physiol 1995; 268:F885-898
Kriz and Bachmann J Cardiovasc Pharm 1985; 7: S24-30;Elger, et al., Adv Anat Embryol Cell Biol 1998; 139:1-98
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Ang II vs. L-NAME-induced Hypertension
• Ang II-induced hypertension exhibits a diminished susceptibility to renal injury as compared to L-NAME-induced hypertension.
• BP – RBF relationships in conscious Ang II-infused rats suggests this is likely due to reduced transmission of elevated systemic BP to the renal microvasculature.
Polichnowski, et al. Am J Physiol 2015; 308:F252-F260
Ren
al D
amag
e Sc
ore
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100 120 140 160 180 200
Systolic BP, mmHg
Ren
al D
amag
e
Hypertensive Renal Damage(Impact of Susceptibility and BP Differences)
Griffin KA and Bidani AK, Clin J Am Soc Nephrol 2006; 1(5):1054-1065
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Anil Bidani, M.D.Maria Picken, M.D., Ph.D. Loyola University Med Ctr.and Hines VA Hospital
Aaron Polichnowski, Ph.D.East Tennessee State University & James H. Quillen VA Hospital
Rodger Loutzenhiser, Ph.D.University of Calgary
Manjeri Venkatachalam, M.D.Univ. of Texas, San Antonio
Geoffrey Williamson, Ph.D.Illinois Institute of Technology
Collaborators
Grant Support: NIH Grants: DK-40426 and DK-61653 Department of Veterans Affairs Merit Review Award
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Renal Circulation: Pressure Profiles
Ofstad and Aukland: Renal Circulation. The Kidney: Physiology and Pathophysiology. (Eds). Seldin and Giebisch. 1985
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Griffin et al, JASN 2000; 11:497- 506
MICROPUNCTURE AND MORPHOMETRIC DATA AT 3 WEEKS
AP GFR SNGFR PGC Kf Glom Vol mmHg ml/min/kg nl/min mmHg nl/sec/mmHg µ-3x10-6
Sham 105+2 39+0.3 38.4 46.3+0.8 0.04+0.002 1.1+0.04(n=10)
RK-NX 5/6 104+3 2.7+0.2* 78.3* 50.5+0.9* 0.06+0.008* 1.7+0.1*(n=10)
RK-I 5/6 136+3*δ 2.2+0.3* 72.9* 55.6+1.1*δ 0.05+0.006 1.9+0.1*(n=10)
*p < .01 compared to control, δ p < .01 compared to RK-NX 5/6
Pathogenesis of Glomerulosclerosisin Renal Mass Reduction Models
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Griffin et al, JASN 2000; 11:497- 506
MICROPUNCTURE AND MORPHOMETRIC DATA AT 3 WEEKSAP GFR SNGFR PGC Kf Glom Vol
mmHg ml/min/kg nl/min mmHg nl/sec/mmHg µ-3x10-6
Sham 105+2 39+0.3 38.4 46.3+0.8 0.04+0.002 1.1+0.04(n=10)
RK-NX 5/6 104+3 2.7+0.2* 78.3* 50.5+0.9* 0.06+0.008* 1.7+0.1*(n=10)
RK-I 5/6 136+3*δ 2.2+0.3* 72.9* 55.6+1.1*δ 0.05+0.006 1.9+0.1*(n=10)
*p < .01 compared to control, δ p < .01 compared to RK-NX 5/6
Pathogenesis of Glomerulosclerosisin Renal Mass Reduction Models
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Griffin et al, JASN 2000; 11:497- 506
MICROPUNCTURE AND MORPHOMETRIC DATA AT 3 WEEKSAP GFR SNGFR PGC Kf Glom Vol
mmHg ml/min/kg nl/min mmHg nl/sec/mmHg µ-3x10-6
Sham 105+2 39+0.3 38.4 46.3+0.8 0.04+0.002 1.1+0.04(n=10)
RK-NX 5/6 104+3 2.7+0.2* 78.3* 50.5+0.9* 0.06+0.008* 1.7+0.1*(n=10)
RK-I 5/6 136+3*δ 2.2+0.3* 72.9* 55.6+1.1*δ 0.05+0.006 1.9+0.1*(n=10)
*p < .01 compared to control, δ p < .01 compared to RK-NX 5/6
Pathogenesis of Glomerulosclerosisin Renal Mass Reduction Models
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Griffin et al, JASN 2000; 11:497- 506
MICROPUNCTURE AND MORPHOMETRIC DATA AT 3 WEEKSAP GFR SNGFR PGC Kf Glom Vol
mmHg ml/min/kg nl/min mmHg nl/sec/mmHg µ-3x10-6
Sham 105+2 39+0.3 38.4 46.3+0.8 0.04+0.002 1.1+0.04(n=10)
RK-NX 5/6 104+3 2.7+0.2* 78.3* 50.5+0.9* 0.06+0.008* 1.7+0.1*(n=10)
RK-I 5/6 136+3*δ 2.2+0.3* 72.9* 55.6+1.1*δ 0.05+0.006 1.9+0.1*(n=10)
*p < .01 compared to control, δ p < .01 compared to RK-NX 5/6
Pathogenesis of Glomerulosclerosisin Renal Mass Reduction Models
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Hypertension 65:510-516, 2015