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Kidney Hypoxia, Attributable to Increased Oxygen Consumption, Induces Nephropathy Independently of Hyperglycemia and Oxidative Stress

Diabetic nephropathy is strongly associated with both increased oxidative stress and kidney tissue hypoxia. The increased oxidative stress causes increased kidney oxygen consumption resulting in kidney tissue hypoxia. To date, it has been difficult to determine the role of kidney hypoxia, per se, fo... Full description

Journal Title: Hypertension (Dallas Tex. 1979), 2013-11, Vol.62 (5), p.914-919
Main Author: Friederich-Persson, Malou
Other Authors: Thörn, Erik , Hansell, Peter , Nangaku, Masaomi , Levin, Max , Palm, Fredrik
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Hagerstown, MD: American Heart Association, Inc
ID: ISSN: 0194-911X
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recordid: cdi_swepub_primary_oai_gup_ub_gu_se_194302
title: Kidney Hypoxia, Attributable to Increased Oxygen Consumption, Induces Nephropathy Independently of Hyperglycemia and Oxidative Stress
format: Article
creator:
  • Friederich-Persson, Malou
  • Thörn, Erik
  • Hansell, Peter
  • Nangaku, Masaomi
  • Levin, Max
  • Palm, Fredrik
subjects:
  • Animals
  • Arterial hypertension. Arterial hypotension
  • Biological and medical sciences
  • Blood and lymphatic vessels
  • Cardiology. Vascular system
  • cell hypoxia
  • cell hypoxia
  • chronic kidney disease
  • dinitrophenols
  • kidney
  • nephropathy
  • chronic tubulointerstitial
  • oxygen consumption
  • uncoupling agents
  • chronic kidney disease
  • chronic tubulointerstitial
  • DIABETIC-NEPHROPATHY
  • DINITROPHENOL
  • dinitrophenols
  • Dinitrophenols - pharmacology
  • ENERGY-METABOLISM
  • Glucose - metabolism
  • Glycogen - metabolism
  • Hyperglycemia - metabolism
  • Hyperglycemia - pathology
  • Hypoxia - metabolism
  • Hypoxia - pathology
  • INTRARENAL OXYGEN
  • ISCHEMIC-INJURY
  • kidney
  • Kidney - drug effects
  • Kidney - metabolism
  • Kidney - pathology
  • Kidney Diseases - metabolism
  • Kidney Diseases - pathology
  • Kidneys
  • Male
  • Medical and Health Sciences
  • Medical sciences
  • MEDICIN
  • Medicin och hälsovetenskap
  • MEDICINE
  • Mitochondria - drug effects
  • Mitochondria - metabolism
  • Mitochondria - pathology
  • Nephrology. Urinary tract diseases
  • Nephropathies. Renovascular diseases. Renal failure
  • nephropathy
  • Oxidative Stress - drug effects
  • Oxidative Stress - physiology
  • oxygen consumption
  • Oxygen Consumption - drug effects
  • Oxygen Consumption - physiology
  • RAT-KIDNEY
  • Rats
  • Rats, Sprague-Dawley
  • Renal Circulation - physiology
  • Renal failure
  • SODIUM-REABSORPTION
  • STAGE RENAL-DISEASE
  • TUBULAR EPITHELIAL-CELLS
  • uncoupling agents
  • Uncoupling Agents - pharmacology
  • Urinary system involvement in other diseases. Miscellaneous
  • Urologi och njurmedicin
  • Urology and Nephrology
  • Vimentin - metabolism
  • VIMENTIN EXPRESSION
ispartof: Hypertension (Dallas, Tex. 1979), 2013-11, Vol.62 (5), p.914-919
description: Diabetic nephropathy is strongly associated with both increased oxidative stress and kidney tissue hypoxia. The increased oxidative stress causes increased kidney oxygen consumption resulting in kidney tissue hypoxia. To date, it has been difficult to determine the role of kidney hypoxia, per se, for the development of nephropathy. We tested the hypothesis that kidney hypoxia, without confounding factors such as hyperglycemia or elevated oxidative stress, results in nephropathy. To induce kidney hypoxia, dinitrophenol (30 mg per day per kg bodyweight by gavage), a mitochondrial uncoupler that increases oxygen consumption and causes kidney hypoxia, was administered for 30 consecutive days to rats. Thereafter, glomerular filtration rate, renal blood flow, kidney oxygen consumption, kidney oxygen tension, kidney concentrations of glucose and glycogen, markers of oxidative stress, urinary protein excretion, and histological findings were determined and compared with vehicle-treated controls. Dinitrophenol did not affect arterial blood pressure, renal blood flow, glomerular filtration rate, blood glucose, or markers of oxidative stress but increased kidney oxygen consumption, and reduced cortical and medullary concentrations of glucose and glycogen, and resulted in intrarenal tissue hypoxia. Furthermore, dinitrophenol treatment increased urinary protein excretion, kidney vimentin expression, and infiltration of inflammatory cells. In conclusion, increased mitochondrial oxygen consumption results in kidney hypoxia and subsequent nephropathy. Importantly, these results demonstrate that kidney tissue hypoxia, per se, without confounding hyperglycemia or oxidative stress, may be sufficient to initiate the development of nephropathy and therefore demonstrate a new interventional target for treating kidney disease.
language: eng
source:
identifier: ISSN: 0194-911X
fulltext: no_fulltext
issn:
  • 0194-911X
  • 1524-4563
  • 1524-4563
url: Link


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titleKidney Hypoxia, Attributable to Increased Oxygen Consumption, Induces Nephropathy Independently of Hyperglycemia and Oxidative Stress
creatorFriederich-Persson, Malou ; Thörn, Erik ; Hansell, Peter ; Nangaku, Masaomi ; Levin, Max ; Palm, Fredrik
creatorcontribFriederich-Persson, Malou ; Thörn, Erik ; Hansell, Peter ; Nangaku, Masaomi ; Levin, Max ; Palm, Fredrik ; Sahlgrenska akademin ; Wallenberg Laboratory ; Wallenberglaboratoriet ; Göteborgs universitet ; Gothenburg University ; Sahlgrenska Academy
descriptionDiabetic nephropathy is strongly associated with both increased oxidative stress and kidney tissue hypoxia. The increased oxidative stress causes increased kidney oxygen consumption resulting in kidney tissue hypoxia. To date, it has been difficult to determine the role of kidney hypoxia, per se, for the development of nephropathy. We tested the hypothesis that kidney hypoxia, without confounding factors such as hyperglycemia or elevated oxidative stress, results in nephropathy. To induce kidney hypoxia, dinitrophenol (30 mg per day per kg bodyweight by gavage), a mitochondrial uncoupler that increases oxygen consumption and causes kidney hypoxia, was administered for 30 consecutive days to rats. Thereafter, glomerular filtration rate, renal blood flow, kidney oxygen consumption, kidney oxygen tension, kidney concentrations of glucose and glycogen, markers of oxidative stress, urinary protein excretion, and histological findings were determined and compared with vehicle-treated controls. Dinitrophenol did not affect arterial blood pressure, renal blood flow, glomerular filtration rate, blood glucose, or markers of oxidative stress but increased kidney oxygen consumption, and reduced cortical and medullary concentrations of glucose and glycogen, and resulted in intrarenal tissue hypoxia. Furthermore, dinitrophenol treatment increased urinary protein excretion, kidney vimentin expression, and infiltration of inflammatory cells. In conclusion, increased mitochondrial oxygen consumption results in kidney hypoxia and subsequent nephropathy. Importantly, these results demonstrate that kidney tissue hypoxia, per se, without confounding hyperglycemia or oxidative stress, may be sufficient to initiate the development of nephropathy and therefore demonstrate a new interventional target for treating kidney disease.
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0ISSN: 0194-911X
1ISSN: 1524-4563
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3DOI: 10.1161/HYPERTENSIONAHA.113.01425
4PMID: 24019401
5CODEN: HPRTDN
languageeng
publisherHagerstown, MD: American Heart Association, Inc
subjectAnimals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; cell hypoxia ; cell hypoxia; chronic kidney disease; dinitrophenols; kidney; nephropathy; chronic tubulointerstitial; oxygen consumption; uncoupling agents ; chronic kidney disease ; chronic tubulointerstitial ; DIABETIC-NEPHROPATHY ; DINITROPHENOL ; dinitrophenols ; Dinitrophenols - pharmacology ; ENERGY-METABOLISM ; Glucose - metabolism ; Glycogen - metabolism ; Hyperglycemia - metabolism ; Hyperglycemia - pathology ; Hypoxia - metabolism ; Hypoxia - pathology ; INTRARENAL OXYGEN ; ISCHEMIC-INJURY ; kidney ; Kidney - drug effects ; Kidney - metabolism ; Kidney - pathology ; Kidney Diseases - metabolism ; Kidney Diseases - pathology ; Kidneys ; Male ; Medical and Health Sciences ; Medical sciences ; MEDICIN ; Medicin och hälsovetenskap ; MEDICINE ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondria - pathology ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; nephropathy ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; oxygen consumption ; Oxygen Consumption - drug effects ; Oxygen Consumption - physiology ; RAT-KIDNEY ; Rats ; Rats, Sprague-Dawley ; Renal Circulation - physiology ; Renal failure ; SODIUM-REABSORPTION ; STAGE RENAL-DISEASE ; TUBULAR EPITHELIAL-CELLS ; uncoupling agents ; Uncoupling Agents - pharmacology ; Urinary system involvement in other diseases. Miscellaneous ; Urologi och njurmedicin ; Urology and Nephrology ; Vimentin - metabolism ; VIMENTIN EXPRESSION
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0Friederich-Persson, Malou
1Thörn, Erik
2Hansell, Peter
3Nangaku, Masaomi
4Levin, Max
5Palm, Fredrik
6Sahlgrenska akademin
7Wallenberg Laboratory
8Wallenberglaboratoriet
9Göteborgs universitet
10Gothenburg University
11Sahlgrenska Academy
title
0Kidney Hypoxia, Attributable to Increased Oxygen Consumption, Induces Nephropathy Independently of Hyperglycemia and Oxidative Stress
1Hypertension (Dallas, Tex. 1979)
addtitleHypertension
descriptionDiabetic nephropathy is strongly associated with both increased oxidative stress and kidney tissue hypoxia. The increased oxidative stress causes increased kidney oxygen consumption resulting in kidney tissue hypoxia. To date, it has been difficult to determine the role of kidney hypoxia, per se, for the development of nephropathy. We tested the hypothesis that kidney hypoxia, without confounding factors such as hyperglycemia or elevated oxidative stress, results in nephropathy. To induce kidney hypoxia, dinitrophenol (30 mg per day per kg bodyweight by gavage), a mitochondrial uncoupler that increases oxygen consumption and causes kidney hypoxia, was administered for 30 consecutive days to rats. Thereafter, glomerular filtration rate, renal blood flow, kidney oxygen consumption, kidney oxygen tension, kidney concentrations of glucose and glycogen, markers of oxidative stress, urinary protein excretion, and histological findings were determined and compared with vehicle-treated controls. Dinitrophenol did not affect arterial blood pressure, renal blood flow, glomerular filtration rate, blood glucose, or markers of oxidative stress but increased kidney oxygen consumption, and reduced cortical and medullary concentrations of glucose and glycogen, and resulted in intrarenal tissue hypoxia. Furthermore, dinitrophenol treatment increased urinary protein excretion, kidney vimentin expression, and infiltration of inflammatory cells. In conclusion, increased mitochondrial oxygen consumption results in kidney hypoxia and subsequent nephropathy. Importantly, these results demonstrate that kidney tissue hypoxia, per se, without confounding hyperglycemia or oxidative stress, may be sufficient to initiate the development of nephropathy and therefore demonstrate a new interventional target for treating kidney disease.
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0Animals
1Arterial hypertension. Arterial hypotension
2Biological and medical sciences
3Blood and lymphatic vessels
4Cardiology. Vascular system
5cell hypoxia
6cell hypoxia; chronic kidney disease; dinitrophenols; kidney; nephropathy; chronic tubulointerstitial; oxygen consumption; uncoupling agents
7chronic kidney disease
8chronic tubulointerstitial
9DIABETIC-NEPHROPATHY
10DINITROPHENOL
11dinitrophenols
12Dinitrophenols - pharmacology
13ENERGY-METABOLISM
14Glucose - metabolism
15Glycogen - metabolism
16Hyperglycemia - metabolism
17Hyperglycemia - pathology
18Hypoxia - metabolism
19Hypoxia - pathology
20INTRARENAL OXYGEN
21ISCHEMIC-INJURY
22kidney
23Kidney - drug effects
24Kidney - metabolism
25Kidney - pathology
26Kidney Diseases - metabolism
27Kidney Diseases - pathology
28Kidneys
29Male
30Medical and Health Sciences
31Medical sciences
32MEDICIN
33Medicin och hälsovetenskap
34MEDICINE
35Mitochondria - drug effects
36Mitochondria - metabolism
37Mitochondria - pathology
38Nephrology. Urinary tract diseases
39Nephropathies. Renovascular diseases. Renal failure
40nephropathy
41Oxidative Stress - drug effects
42Oxidative Stress - physiology
43oxygen consumption
44Oxygen Consumption - drug effects
45Oxygen Consumption - physiology
46RAT-KIDNEY
47Rats
48Rats, Sprague-Dawley
49Renal Circulation - physiology
50Renal failure
51SODIUM-REABSORPTION
52STAGE RENAL-DISEASE
53TUBULAR EPITHELIAL-CELLS
54uncoupling agents
55Uncoupling Agents - pharmacology
56Urinary system involvement in other diseases. Miscellaneous
57Urologi och njurmedicin
58Urology and Nephrology
59Vimentin - metabolism
60VIMENTIN EXPRESSION
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startdate201311
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1Thörn, Erik
2Hansell, Peter
3Nangaku, Masaomi
4Levin, Max
5Palm, Fredrik
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titleKidney Hypoxia, Attributable to Increased Oxygen Consumption, Induces Nephropathy Independently of Hyperglycemia and Oxidative Stress
authorFriederich-Persson, Malou ; Thörn, Erik ; Hansell, Peter ; Nangaku, Masaomi ; Levin, Max ; Palm, Fredrik
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1Arterial hypertension. Arterial hypotension
2Biological and medical sciences
3Blood and lymphatic vessels
4Cardiology. Vascular system
5cell hypoxia
6cell hypoxia; chronic kidney disease; dinitrophenols; kidney; nephropathy; chronic tubulointerstitial; oxygen consumption; uncoupling agents
7chronic kidney disease
8chronic tubulointerstitial
9DIABETIC-NEPHROPATHY
10DINITROPHENOL
11dinitrophenols
12Dinitrophenols - pharmacology
13ENERGY-METABOLISM
14Glucose - metabolism
15Glycogen - metabolism
16Hyperglycemia - metabolism
17Hyperglycemia - pathology
18Hypoxia - metabolism
19Hypoxia - pathology
20INTRARENAL OXYGEN
21ISCHEMIC-INJURY
22kidney
23Kidney - drug effects
24Kidney - metabolism
25Kidney - pathology
26Kidney Diseases - metabolism
27Kidney Diseases - pathology
28Kidneys
29Male
30Medical and Health Sciences
31Medical sciences
32MEDICIN
33Medicin och hälsovetenskap
34MEDICINE
35Mitochondria - drug effects
36Mitochondria - metabolism
37Mitochondria - pathology
38Nephrology. Urinary tract diseases
39Nephropathies. Renovascular diseases. Renal failure
40nephropathy
41Oxidative Stress - drug effects
42Oxidative Stress - physiology
43oxygen consumption
44Oxygen Consumption - drug effects
45Oxygen Consumption - physiology
46RAT-KIDNEY
47Rats
48Rats, Sprague-Dawley
49Renal Circulation - physiology
50Renal failure
51SODIUM-REABSORPTION
52STAGE RENAL-DISEASE
53TUBULAR EPITHELIAL-CELLS
54uncoupling agents
55Uncoupling Agents - pharmacology
56Urinary system involvement in other diseases. Miscellaneous
57Urologi och njurmedicin
58Urology and Nephrology
59Vimentin - metabolism
60VIMENTIN EXPRESSION
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1Thörn, Erik
2Hansell, Peter
3Nangaku, Masaomi
4Levin, Max
5Palm, Fredrik
6Sahlgrenska akademin
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8Wallenberglaboratoriet
9Göteborgs universitet
10Gothenburg University
11Sahlgrenska Academy
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atitleKidney Hypoxia, Attributable to Increased Oxygen Consumption, Induces Nephropathy Independently of Hyperglycemia and Oxidative Stress
jtitleHypertension (Dallas, Tex. 1979)
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abstractDiabetic nephropathy is strongly associated with both increased oxidative stress and kidney tissue hypoxia. The increased oxidative stress causes increased kidney oxygen consumption resulting in kidney tissue hypoxia. To date, it has been difficult to determine the role of kidney hypoxia, per se, for the development of nephropathy. We tested the hypothesis that kidney hypoxia, without confounding factors such as hyperglycemia or elevated oxidative stress, results in nephropathy. To induce kidney hypoxia, dinitrophenol (30 mg per day per kg bodyweight by gavage), a mitochondrial uncoupler that increases oxygen consumption and causes kidney hypoxia, was administered for 30 consecutive days to rats. Thereafter, glomerular filtration rate, renal blood flow, kidney oxygen consumption, kidney oxygen tension, kidney concentrations of glucose and glycogen, markers of oxidative stress, urinary protein excretion, and histological findings were determined and compared with vehicle-treated controls. Dinitrophenol did not affect arterial blood pressure, renal blood flow, glomerular filtration rate, blood glucose, or markers of oxidative stress but increased kidney oxygen consumption, and reduced cortical and medullary concentrations of glucose and glycogen, and resulted in intrarenal tissue hypoxia. Furthermore, dinitrophenol treatment increased urinary protein excretion, kidney vimentin expression, and infiltration of inflammatory cells. In conclusion, increased mitochondrial oxygen consumption results in kidney hypoxia and subsequent nephropathy. Importantly, these results demonstrate that kidney tissue hypoxia, per se, without confounding hyperglycemia or oxidative stress, may be sufficient to initiate the development of nephropathy and therefore demonstrate a new interventional target for treating kidney disease.
copHagerstown, MD
pubAmerican Heart Association, Inc
pmid24019401
doi10.1161/HYPERTENSIONAHA.113.01425
oafree_for_read