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Progression of Chronic Kidney Disease After Acute Kidney Injury: Role of Self-Perpetuating Versus Hemodynamic-Induced Fibrosis

The relative contribution of self-perpetuating versus hemodynamic-induced fibrosis to the progression of chronic kidney disease (CKD) after acute kidney injury (AKI) is unclear. In the present study, male Sprague-Dawley rats underwent right uninephrectomy and were instrumented with a blood pressure... Full description

Journal Title: Hypertension (Dallas Tex. 1979), 2016-08-22, Vol.68 (4), p.921-928
Main Author: Picken, Maria
Other Authors: Long, Jianrui , Williamson, Geoffrey A , Polichnowski, Aaron J
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: United States: American Heart Association, Inc
ID: ISSN: 0194-911X
Link: https://www.ncbi.nlm.nih.gov/pubmed/27550923
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recordid: cdi_proquest_miscellaneous_1818331739
title: Progression of Chronic Kidney Disease After Acute Kidney Injury: Role of Self-Perpetuating Versus Hemodynamic-Induced Fibrosis
format: Article
creator:
  • Picken, Maria
  • Long, Jianrui
  • Williamson, Geoffrey A
  • Polichnowski, Aaron J
subjects:
  • Acute Kidney Injury - complications
  • Acute Kidney Injury - pathology
  • Acute Kidney Injury - physiopathology
  • Analysis of Variance
  • Animals
  • Blood Pressure Determination
  • Disease Models, Animal
  • Disease Progression
  • Fibrosis - pathology
  • Glomerular Filtration Rate - physiology
  • Glomerulosclerosis, Focal Segmental - pathology
  • Glomerulosclerosis, Focal Segmental - physiopathology
  • Hemodynamics - physiology
  • Male
  • Nephritis, Interstitial - pathology
  • Nephritis, Interstitial - physiopathology
  • Proteinuria - physiopathology
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Renal Insufficiency, Chronic - etiology
  • Renal Insufficiency, Chronic - pathology
  • Renal Insufficiency, Chronic - physiopathology
  • Risk Assessment
  • Statistics, Nonparametric
ispartof: Hypertension (Dallas, Tex. 1979), 2016-08-22, Vol.68 (4), p.921-928
description: The relative contribution of self-perpetuating versus hemodynamic-induced fibrosis to the progression of chronic kidney disease (CKD) after acute kidney injury (AKI) is unclear. In the present study, male Sprague-Dawley rats underwent right uninephrectomy and were instrumented with a blood pressure radiotelemeter. Two weeks later, separate groups of rats were subjected to 40 minutes renal ischemia–reperfusion or sham surgery and followed up for 4 or 16 weeks to determine the extent to which glomerulosclerosis and tubulointerstitial fibrosis as a result of the AKI–CKD transition (ie, at 4 weeks post AKI) change over time during the progression of CKD (ie, at 16 weeks post AKI). On average, tubulointerstitial fibrosis was ≈3-fold lower (P
language: eng
source:
identifier: ISSN: 0194-911X
fulltext: no_fulltext
issn:
  • 0194-911X
  • 1524-4563
url: Link


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titleProgression of Chronic Kidney Disease After Acute Kidney Injury: Role of Self-Perpetuating Versus Hemodynamic-Induced Fibrosis
creatorPicken, Maria ; Long, Jianrui ; Williamson, Geoffrey A ; Polichnowski, Aaron J
creatorcontribPicken, Maria ; Long, Jianrui ; Williamson, Geoffrey A ; Polichnowski, Aaron J
descriptionThe relative contribution of self-perpetuating versus hemodynamic-induced fibrosis to the progression of chronic kidney disease (CKD) after acute kidney injury (AKI) is unclear. In the present study, male Sprague-Dawley rats underwent right uninephrectomy and were instrumented with a blood pressure radiotelemeter. Two weeks later, separate groups of rats were subjected to 40 minutes renal ischemia–reperfusion or sham surgery and followed up for 4 or 16 weeks to determine the extent to which glomerulosclerosis and tubulointerstitial fibrosis as a result of the AKI–CKD transition (ie, at 4 weeks post AKI) change over time during the progression of CKD (ie, at 16 weeks post AKI). On average, tubulointerstitial fibrosis was ≈3-fold lower (P<0.05), whereas glomerulosclerosis was ≈6-fold higher (P<0.05) at 16 versus 4 weeks post AKI. At 16 weeks post AKI, marked tubulointerstitial fibrosis was only observed in rats exhibiting marked glomerulosclerosis, proteinuria, and kidney hypertrophy consistent with a hemodynamic pathogenesis of renal injury. Moreover, quantitative analysis between blood pressure and renal injury revealed a clear and modest blood pressure threshold (average 16-week systolic blood pressure of ≈127 mm Hg) for the development of glomerulosclerosis. In summary, modest levels of blood pressure may be playing a substantial role in the progression of renal disease after AKI in settings of preexisting CKD associated with 50% loss of renal mass. In contrast, these data do not support a major role of self-perpetuating tubulointerstitial fibrosis in the progression CKD after AKI in such settings.
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languageeng
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subjectAcute Kidney Injury - complications ; Acute Kidney Injury - pathology ; Acute Kidney Injury - physiopathology ; Analysis of Variance ; Animals ; Blood Pressure Determination ; Disease Models, Animal ; Disease Progression ; Fibrosis - pathology ; Glomerular Filtration Rate - physiology ; Glomerulosclerosis, Focal Segmental - pathology ; Glomerulosclerosis, Focal Segmental - physiopathology ; Hemodynamics - physiology ; Male ; Nephritis, Interstitial - pathology ; Nephritis, Interstitial - physiopathology ; Proteinuria - physiopathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Renal Insufficiency, Chronic - etiology ; Renal Insufficiency, Chronic - pathology ; Renal Insufficiency, Chronic - physiopathology ; Risk Assessment ; Statistics, Nonparametric
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descriptionThe relative contribution of self-perpetuating versus hemodynamic-induced fibrosis to the progression of chronic kidney disease (CKD) after acute kidney injury (AKI) is unclear. In the present study, male Sprague-Dawley rats underwent right uninephrectomy and were instrumented with a blood pressure radiotelemeter. Two weeks later, separate groups of rats were subjected to 40 minutes renal ischemia–reperfusion or sham surgery and followed up for 4 or 16 weeks to determine the extent to which glomerulosclerosis and tubulointerstitial fibrosis as a result of the AKI–CKD transition (ie, at 4 weeks post AKI) change over time during the progression of CKD (ie, at 16 weeks post AKI). On average, tubulointerstitial fibrosis was ≈3-fold lower (P<0.05), whereas glomerulosclerosis was ≈6-fold higher (P<0.05) at 16 versus 4 weeks post AKI. At 16 weeks post AKI, marked tubulointerstitial fibrosis was only observed in rats exhibiting marked glomerulosclerosis, proteinuria, and kidney hypertrophy consistent with a hemodynamic pathogenesis of renal injury. Moreover, quantitative analysis between blood pressure and renal injury revealed a clear and modest blood pressure threshold (average 16-week systolic blood pressure of ≈127 mm Hg) for the development of glomerulosclerosis. In summary, modest levels of blood pressure may be playing a substantial role in the progression of renal disease after AKI in settings of preexisting CKD associated with 50% loss of renal mass. In contrast, these data do not support a major role of self-perpetuating tubulointerstitial fibrosis in the progression CKD after AKI in such settings.
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0Acute Kidney Injury - complications
1Acute Kidney Injury - pathology
2Acute Kidney Injury - physiopathology
3Analysis of Variance
4Animals
5Blood Pressure Determination
6Disease Models, Animal
7Disease Progression
8Fibrosis - pathology
9Glomerular Filtration Rate - physiology
10Glomerulosclerosis, Focal Segmental - pathology
11Glomerulosclerosis, Focal Segmental - physiopathology
12Hemodynamics - physiology
13Male
14Nephritis, Interstitial - pathology
15Nephritis, Interstitial - physiopathology
16Proteinuria - physiopathology
17Random Allocation
18Rats
19Rats, Sprague-Dawley
20Renal Insufficiency, Chronic - etiology
21Renal Insufficiency, Chronic - pathology
22Renal Insufficiency, Chronic - physiopathology
23Risk Assessment
24Statistics, Nonparametric
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21Renal Insufficiency, Chronic - pathology
22Renal Insufficiency, Chronic - physiopathology
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abstractThe relative contribution of self-perpetuating versus hemodynamic-induced fibrosis to the progression of chronic kidney disease (CKD) after acute kidney injury (AKI) is unclear. In the present study, male Sprague-Dawley rats underwent right uninephrectomy and were instrumented with a blood pressure radiotelemeter. Two weeks later, separate groups of rats were subjected to 40 minutes renal ischemia–reperfusion or sham surgery and followed up for 4 or 16 weeks to determine the extent to which glomerulosclerosis and tubulointerstitial fibrosis as a result of the AKI–CKD transition (ie, at 4 weeks post AKI) change over time during the progression of CKD (ie, at 16 weeks post AKI). On average, tubulointerstitial fibrosis was ≈3-fold lower (P<0.05), whereas glomerulosclerosis was ≈6-fold higher (P<0.05) at 16 versus 4 weeks post AKI. At 16 weeks post AKI, marked tubulointerstitial fibrosis was only observed in rats exhibiting marked glomerulosclerosis, proteinuria, and kidney hypertrophy consistent with a hemodynamic pathogenesis of renal injury. Moreover, quantitative analysis between blood pressure and renal injury revealed a clear and modest blood pressure threshold (average 16-week systolic blood pressure of ≈127 mm Hg) for the development of glomerulosclerosis. In summary, modest levels of blood pressure may be playing a substantial role in the progression of renal disease after AKI in settings of preexisting CKD associated with 50% loss of renal mass. In contrast, these data do not support a major role of self-perpetuating tubulointerstitial fibrosis in the progression CKD after AKI in such settings.
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