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Urinary Mitochondrial DNA Copy Number Identifies Chronic Renal Injury in Hypertensive Patients

Mitochondrial injury contributes to renal dysfunction in several models of renal disease, but its involvement in human hypertension remains unknown. Fragments of the mitochondrial genome released from dying cells are considered surrogate markers of mitochondrial injury. We hypothesized that hyperten... Full description

Journal Title: Hypertension (Dallas Tex. 1979), 2016, Vol.68 (2), p.401-410
Main Author: Eirin, Alfonso
Other Authors: Saad, Ahmed , Tang, Hui , Herrmann, Sandra M , Woollard, John R , Lerman, Amir , Textor, Stephen C , Lerman, Lilach O
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/27324229
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4945445
title: Urinary Mitochondrial DNA Copy Number Identifies Chronic Renal Injury in Hypertensive Patients
format: Article
creator:
  • Eirin, Alfonso
  • Saad, Ahmed
  • Tang, Hui
  • Herrmann, Sandra M
  • Woollard, John R
  • Lerman, Amir
  • Textor, Stephen C
  • Lerman, Lilach O
subjects:
  • Acute Kidney Injury - metabolism
  • Acute Kidney Injury - pathology
  • Acute Kidney Injury - physiopathology
  • Aged
  • Article
  • Biomarkers - analysis
  • Biomarkers - urine
  • Blood Pressure Determination - methods
  • DAMPs
  • DNA, Mitochondrial - urine
  • Electron Transport Complex IV - analysis
  • Essential Hypertension
  • Female
  • Hepatitis A Virus Cellular Receptor 1 - analysis
  • Humans
  • Hypertension
  • Hypertension - diagnosis
  • Hypertension - metabolism
  • Hypertension - physiopathology
  • Hypertension, Renovascular - diagnosis
  • Hypertension, Renovascular - metabolism
  • Hypertension, Renovascular - physiopathology
  • Kidney - metabolism
  • Kidney - pathology
  • Kidney - physiopathology
  • KIM-1
  • Lipocalin-2 - analysis
  • Male
  • Middle Aged
  • Mitochondria
  • Mitochondria - pathology
  • NADH Dehydrogenase - analysis
  • NGAL
  • Renal Circulation
  • Statistics as Topic
ispartof: Hypertension (Dallas, Tex. 1979), 2016, Vol.68 (2), p.401-410
description: Mitochondrial injury contributes to renal dysfunction in several models of renal disease, but its involvement in human hypertension remains unknown. Fragments of the mitochondrial genome released from dying cells are considered surrogate markers of mitochondrial injury. We hypothesized that hypertension would be associated with increased urine mitochondrial DNA (mtDNA) copy numbers. We prospectively measured systemic and urinary copy number of the mtDNA genes cytochrome-c oxidase-3 and NADH dehydrogenase subunit-1 by quantitative polymerase chain reaction in essential (n=25) and renovascular (RVH, n=34) hypertensive patients and compared them with healthy volunteers (n=22). Urinary kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin served as indices of renal injury. Renal blood flow and oxygenation were assessed by multidetector computed tomography and blood oxygen level–dependent magnetic resonance imaging. Blood pressure, urinary neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1 were similarly elevated in essential hypertension and RVH, and estimated glomerular filtration rate was lower in RVH versus healthy volunteers and essential hypertension. Renal blood flow was lower in RVH compared with essential hypertension. Urinary mtDNA copy number was higher in hypertension compared with healthy volunteers, directly correlated with urinary neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 and inversely with estimated glomerular filtration rate. In RVH, urinary mtDNA copy number correlated directly with intrarenal hypoxia. Furthermore, in an additional validation cohort, urinary mtDNA copy number was higher in RVH compared with healthy volunteers (n=10 each). The change in serum creatinine levels and estimated glomerular filtration rate 3 months after medical therapy without or with revascularization correlated with the change in urinary mtDNA. Therefore, elevated urinary mtDNA copy numbers in hypertensive patients correlated with markers of renal injury and dysfunction, implicating mitochondrial injury in kidney damage in human hypertension.
language: eng
source:
identifier: ISSN: 0194-911X
fulltext: no_fulltext
issn:
  • 0194-911X
  • 1524-4563
url: Link


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titleUrinary Mitochondrial DNA Copy Number Identifies Chronic Renal Injury in Hypertensive Patients
creatorEirin, Alfonso ; Saad, Ahmed ; Tang, Hui ; Herrmann, Sandra M ; Woollard, John R ; Lerman, Amir ; Textor, Stephen C ; Lerman, Lilach O
creatorcontribEirin, Alfonso ; Saad, Ahmed ; Tang, Hui ; Herrmann, Sandra M ; Woollard, John R ; Lerman, Amir ; Textor, Stephen C ; Lerman, Lilach O
descriptionMitochondrial injury contributes to renal dysfunction in several models of renal disease, but its involvement in human hypertension remains unknown. Fragments of the mitochondrial genome released from dying cells are considered surrogate markers of mitochondrial injury. We hypothesized that hypertension would be associated with increased urine mitochondrial DNA (mtDNA) copy numbers. We prospectively measured systemic and urinary copy number of the mtDNA genes cytochrome-c oxidase-3 and NADH dehydrogenase subunit-1 by quantitative polymerase chain reaction in essential (n=25) and renovascular (RVH, n=34) hypertensive patients and compared them with healthy volunteers (n=22). Urinary kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin served as indices of renal injury. Renal blood flow and oxygenation were assessed by multidetector computed tomography and blood oxygen level–dependent magnetic resonance imaging. Blood pressure, urinary neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1 were similarly elevated in essential hypertension and RVH, and estimated glomerular filtration rate was lower in RVH versus healthy volunteers and essential hypertension. Renal blood flow was lower in RVH compared with essential hypertension. Urinary mtDNA copy number was higher in hypertension compared with healthy volunteers, directly correlated with urinary neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 and inversely with estimated glomerular filtration rate. In RVH, urinary mtDNA copy number correlated directly with intrarenal hypoxia. Furthermore, in an additional validation cohort, urinary mtDNA copy number was higher in RVH compared with healthy volunteers (n=10 each). The change in serum creatinine levels and estimated glomerular filtration rate 3 months after medical therapy without or with revascularization correlated with the change in urinary mtDNA. Therefore, elevated urinary mtDNA copy numbers in hypertensive patients correlated with markers of renal injury and dysfunction, implicating mitochondrial injury in kidney damage in human hypertension.
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languageeng
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subjectAcute Kidney Injury - metabolism ; Acute Kidney Injury - pathology ; Acute Kidney Injury - physiopathology ; Aged ; Article ; Biomarkers - analysis ; Biomarkers - urine ; Blood Pressure Determination - methods ; DAMPs ; DNA, Mitochondrial - urine ; Electron Transport Complex IV - analysis ; Essential Hypertension ; Female ; Hepatitis A Virus Cellular Receptor 1 - analysis ; Humans ; Hypertension ; Hypertension - diagnosis ; Hypertension - metabolism ; Hypertension - physiopathology ; Hypertension, Renovascular - diagnosis ; Hypertension, Renovascular - metabolism ; Hypertension, Renovascular - physiopathology ; Kidney - metabolism ; Kidney - pathology ; Kidney - physiopathology ; KIM-1 ; Lipocalin-2 - analysis ; Male ; Middle Aged ; Mitochondria ; Mitochondria - pathology ; NADH Dehydrogenase - analysis ; NGAL ; Renal Circulation ; Statistics as Topic
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1Saad, Ahmed
2Tang, Hui
3Herrmann, Sandra M
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5Lerman, Amir
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7Lerman, Lilach O
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0Urinary Mitochondrial DNA Copy Number Identifies Chronic Renal Injury in Hypertensive Patients
1Hypertension (Dallas, Tex. 1979)
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descriptionMitochondrial injury contributes to renal dysfunction in several models of renal disease, but its involvement in human hypertension remains unknown. Fragments of the mitochondrial genome released from dying cells are considered surrogate markers of mitochondrial injury. We hypothesized that hypertension would be associated with increased urine mitochondrial DNA (mtDNA) copy numbers. We prospectively measured systemic and urinary copy number of the mtDNA genes cytochrome-c oxidase-3 and NADH dehydrogenase subunit-1 by quantitative polymerase chain reaction in essential (n=25) and renovascular (RVH, n=34) hypertensive patients and compared them with healthy volunteers (n=22). Urinary kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin served as indices of renal injury. Renal blood flow and oxygenation were assessed by multidetector computed tomography and blood oxygen level–dependent magnetic resonance imaging. Blood pressure, urinary neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1 were similarly elevated in essential hypertension and RVH, and estimated glomerular filtration rate was lower in RVH versus healthy volunteers and essential hypertension. Renal blood flow was lower in RVH compared with essential hypertension. Urinary mtDNA copy number was higher in hypertension compared with healthy volunteers, directly correlated with urinary neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 and inversely with estimated glomerular filtration rate. In RVH, urinary mtDNA copy number correlated directly with intrarenal hypoxia. Furthermore, in an additional validation cohort, urinary mtDNA copy number was higher in RVH compared with healthy volunteers (n=10 each). The change in serum creatinine levels and estimated glomerular filtration rate 3 months after medical therapy without or with revascularization correlated with the change in urinary mtDNA. Therefore, elevated urinary mtDNA copy numbers in hypertensive patients correlated with markers of renal injury and dysfunction, implicating mitochondrial injury in kidney damage in human hypertension.
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0Acute Kidney Injury - metabolism
1Acute Kidney Injury - pathology
2Acute Kidney Injury - physiopathology
3Aged
4Article
5Biomarkers - analysis
6Biomarkers - urine
7Blood Pressure Determination - methods
8DAMPs
9DNA, Mitochondrial - urine
10Electron Transport Complex IV - analysis
11Essential Hypertension
12Female
13Hepatitis A Virus Cellular Receptor 1 - analysis
14Humans
15Hypertension
16Hypertension - diagnosis
17Hypertension - metabolism
18Hypertension - physiopathology
19Hypertension, Renovascular - diagnosis
20Hypertension, Renovascular - metabolism
21Hypertension, Renovascular - physiopathology
22Kidney - metabolism
23Kidney - pathology
24Kidney - physiopathology
25KIM-1
26Lipocalin-2 - analysis
27Male
28Middle Aged
29Mitochondria
30Mitochondria - pathology
31NADH Dehydrogenase - analysis
32NGAL
33Renal Circulation
34Statistics as Topic
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titleUrinary Mitochondrial DNA Copy Number Identifies Chronic Renal Injury in Hypertensive Patients
authorEirin, Alfonso ; Saad, Ahmed ; Tang, Hui ; Herrmann, Sandra M ; Woollard, John R ; Lerman, Amir ; Textor, Stephen C ; Lerman, Lilach O
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7Blood Pressure Determination - methods
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31NADH Dehydrogenase - analysis
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1Saad, Ahmed
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jtitleHypertension (Dallas, Tex. 1979)
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abstractMitochondrial injury contributes to renal dysfunction in several models of renal disease, but its involvement in human hypertension remains unknown. Fragments of the mitochondrial genome released from dying cells are considered surrogate markers of mitochondrial injury. We hypothesized that hypertension would be associated with increased urine mitochondrial DNA (mtDNA) copy numbers. We prospectively measured systemic and urinary copy number of the mtDNA genes cytochrome-c oxidase-3 and NADH dehydrogenase subunit-1 by quantitative polymerase chain reaction in essential (n=25) and renovascular (RVH, n=34) hypertensive patients and compared them with healthy volunteers (n=22). Urinary kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin served as indices of renal injury. Renal blood flow and oxygenation were assessed by multidetector computed tomography and blood oxygen level–dependent magnetic resonance imaging. Blood pressure, urinary neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1 were similarly elevated in essential hypertension and RVH, and estimated glomerular filtration rate was lower in RVH versus healthy volunteers and essential hypertension. Renal blood flow was lower in RVH compared with essential hypertension. Urinary mtDNA copy number was higher in hypertension compared with healthy volunteers, directly correlated with urinary neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 and inversely with estimated glomerular filtration rate. In RVH, urinary mtDNA copy number correlated directly with intrarenal hypoxia. Furthermore, in an additional validation cohort, urinary mtDNA copy number was higher in RVH compared with healthy volunteers (n=10 each). The change in serum creatinine levels and estimated glomerular filtration rate 3 months after medical therapy without or with revascularization correlated with the change in urinary mtDNA. Therefore, elevated urinary mtDNA copy numbers in hypertensive patients correlated with markers of renal injury and dysfunction, implicating mitochondrial injury in kidney damage in human hypertension.
copUnited States
pubAmerican Heart Association, Inc
pmid27324229
doi10.1161/HYPERTENSIONAHA.116.07849
oafree_for_read