Association between Mitochondrial DNA Copy Number in Peripheral Blood and Incident CKD in the Atherosclerosis Risk in Communities Study

Mitochondrial dysfunction in kidney cells has been implicated in the pathogenesis of CKD. Mitochondrial DNA (mtDNA) copy number is a surrogate measure of mitochondrial function, and higher mtDNA copy number in peripheral blood has been associated with lower risk of two important risk factors for CKD...

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Vydáno v:	Journal of the American Society of Nephrology Ročník 27; číslo 8; s. 2467
Hlavní autoři:	Tin, Adrienne, Grams, Morgan E, Ashar, Foram N, Lane, John A, Rosenberg, Avi Z, Grove, Megan L, Boerwinkle, Eric, Selvin, Elizabeth, Coresh, Josef, Pankratz, Nathan, Arking, Dan E
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States 01.08.2016
Témata:	Aged Atherosclerosis - complications DNA Copy Number Variations DNA, Mitochondrial - blood DNA, Mitochondrial - genetics Female Humans Male Middle Aged Prospective Studies Renal Insufficiency, Chronic - blood Renal Insufficiency, Chronic - epidemiology Renal Insufficiency, Chronic - etiology Risk Factors chronic kidney disease epidemiology and outcomes renal function decline mitochondria
ISSN:	1533-3450, 1533-3450
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Abstract	Mitochondrial dysfunction in kidney cells has been implicated in the pathogenesis of CKD. Mitochondrial DNA (mtDNA) copy number is a surrogate measure of mitochondrial function, and higher mtDNA copy number in peripheral blood has been associated with lower risk of two important risk factors for CKD progression, diabetes and microalbuminuria. We evaluated whether mtDNA copy number in peripheral blood associates with incident CKD in a population-based cohort of middle-aged adults. We estimated mtDNA copy number using 25 high-quality mitochondrial single nucleotide polymorphisms from the Affymetrix 6.0 array. Among 9058 participants, those with higher mtDNA copy number had a lower rate of prevalent diabetes and lower C-reactive protein levels and white blood cell counts. Baseline eGFR did not differ significantly by mtDNA copy number. Over a median follow-up of 19.6 years, 1490 participants developed CKD. Higher mtDNA copy number associated with lower risk of incident CKD (highest versus lowest quartile: hazard ratio 0.65; 95% confidence interval, 0.56 to 0.75; P<0.001) after adjusting for age, sex, and race. After adjusting for additional risk factors of CKD, including prevalent diabetes, hypertension, C-reactive protein level, and white blood cell count, this association remained significant (highest versus lowest quartile: hazard ratio 0.75; 95% confidence interval, 0.64 to 0.87; P<0.001). In conclusion, higher mtDNA copy number associated with lower incidence of CKD independent of traditional risk factors and inflammation biomarker levels in this cohort. Further research on modifiable factors influencing mtDNA copy number may lead to improvement in the prevention and treatment of CKD.
AbstractList	Mitochondrial dysfunction in kidney cells has been implicated in the pathogenesis of CKD. Mitochondrial DNA (mtDNA) copy number is a surrogate measure of mitochondrial function, and higher mtDNA copy number in peripheral blood has been associated with lower risk of two important risk factors for CKD progression, diabetes and microalbuminuria. We evaluated whether mtDNA copy number in peripheral blood associates with incident CKD in a population-based cohort of middle-aged adults. We estimated mtDNA copy number using 25 high-quality mitochondrial single nucleotide polymorphisms from the Affymetrix 6.0 array. Among 9058 participants, those with higher mtDNA copy number had a lower rate of prevalent diabetes and lower C-reactive protein levels and white blood cell counts. Baseline eGFR did not differ significantly by mtDNA copy number. Over a median follow-up of 19.6 years, 1490 participants developed CKD. Higher mtDNA copy number associated with lower risk of incident CKD (highest versus lowest quartile: hazard ratio 0.65; 95% confidence interval, 0.56 to 0.75; P<0.001) after adjusting for age, sex, and race. After adjusting for additional risk factors of CKD, including prevalent diabetes, hypertension, C-reactive protein level, and white blood cell count, this association remained significant (highest versus lowest quartile: hazard ratio 0.75; 95% confidence interval, 0.64 to 0.87; P<0.001). In conclusion, higher mtDNA copy number associated with lower incidence of CKD independent of traditional risk factors and inflammation biomarker levels in this cohort. Further research on modifiable factors influencing mtDNA copy number may lead to improvement in the prevention and treatment of CKD.Mitochondrial dysfunction in kidney cells has been implicated in the pathogenesis of CKD. Mitochondrial DNA (mtDNA) copy number is a surrogate measure of mitochondrial function, and higher mtDNA copy number in peripheral blood has been associated with lower risk of two important risk factors for CKD progression, diabetes and microalbuminuria. We evaluated whether mtDNA copy number in peripheral blood associates with incident CKD in a population-based cohort of middle-aged adults. We estimated mtDNA copy number using 25 high-quality mitochondrial single nucleotide polymorphisms from the Affymetrix 6.0 array. Among 9058 participants, those with higher mtDNA copy number had a lower rate of prevalent diabetes and lower C-reactive protein levels and white blood cell counts. Baseline eGFR did not differ significantly by mtDNA copy number. Over a median follow-up of 19.6 years, 1490 participants developed CKD. Higher mtDNA copy number associated with lower risk of incident CKD (highest versus lowest quartile: hazard ratio 0.65; 95% confidence interval, 0.56 to 0.75; P<0.001) after adjusting for age, sex, and race. After adjusting for additional risk factors of CKD, including prevalent diabetes, hypertension, C-reactive protein level, and white blood cell count, this association remained significant (highest versus lowest quartile: hazard ratio 0.75; 95% confidence interval, 0.64 to 0.87; P<0.001). In conclusion, higher mtDNA copy number associated with lower incidence of CKD independent of traditional risk factors and inflammation biomarker levels in this cohort. Further research on modifiable factors influencing mtDNA copy number may lead to improvement in the prevention and treatment of CKD. Mitochondrial dysfunction in kidney cells has been implicated in the pathogenesis of CKD. Mitochondrial DNA (mtDNA) copy number is a surrogate measure of mitochondrial function, and higher mtDNA copy number in peripheral blood has been associated with lower risk of two important risk factors for CKD progression, diabetes and microalbuminuria. We evaluated whether mtDNA copy number in peripheral blood associates with incident CKD in a population-based cohort of middle-aged adults. We estimated mtDNA copy number using 25 high-quality mitochondrial single nucleotide polymorphisms from the Affymetrix 6.0 array. Among 9058 participants, those with higher mtDNA copy number had a lower rate of prevalent diabetes and lower C-reactive protein levels and white blood cell counts. Baseline eGFR did not differ significantly by mtDNA copy number. Over a median follow-up of 19.6 years, 1490 participants developed CKD. Higher mtDNA copy number associated with lower risk of incident CKD (highest versus lowest quartile: hazard ratio 0.65; 95% confidence interval, 0.56 to 0.75; P<0.001) after adjusting for age, sex, and race. After adjusting for additional risk factors of CKD, including prevalent diabetes, hypertension, C-reactive protein level, and white blood cell count, this association remained significant (highest versus lowest quartile: hazard ratio 0.75; 95% confidence interval, 0.64 to 0.87; P<0.001). In conclusion, higher mtDNA copy number associated with lower incidence of CKD independent of traditional risk factors and inflammation biomarker levels in this cohort. Further research on modifiable factors influencing mtDNA copy number may lead to improvement in the prevention and treatment of CKD.
Author	Grove, Megan L Boerwinkle, Eric Selvin, Elizabeth Ashar, Foram N Rosenberg, Avi Z Grams, Morgan E Coresh, Josef Pankratz, Nathan Arking, Dan E Lane, John A Tin, Adrienne
Author_xml	– sequence: 1 givenname: Adrienne surname: Tin fullname: Tin, Adrienne email: atin1@jhu.edu organization: Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; atin1@jhu.edu – sequence: 2 givenname: Morgan E surname: Grams fullname: Grams, Morgan E organization: Division of Nephrology, and – sequence: 3 givenname: Foram N surname: Ashar fullname: Ashar, Foram N organization: McKusick-Nathans Institute of Genetic Medicine and Department of Medicine, Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, Maryland – sequence: 4 givenname: John A surname: Lane fullname: Lane, John A organization: Department of Laboratory Medicine and Pathology, University of Minnesota School of Medicine, Minneapolis, Minnesota – sequence: 5 givenname: Avi Z surname: Rosenberg fullname: Rosenberg, Avi Z organization: Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, Federick, Maryland; Children's National Medical Center, Washington, DC; and – sequence: 6 givenname: Megan L surname: Grove fullname: Grove, Megan L organization: Human Genetics Center, The University of Texas Health Science Center at Houston, Houston, Texas – sequence: 7 givenname: Eric surname: Boerwinkle fullname: Boerwinkle, Eric organization: Human Genetics Center, The University of Texas Health Science Center at Houston, Houston, Texas – sequence: 8 givenname: Elizabeth surname: Selvin fullname: Selvin, Elizabeth organization: Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland – sequence: 9 givenname: Josef surname: Coresh fullname: Coresh, Josef organization: Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland – sequence: 10 givenname: Nathan surname: Pankratz fullname: Pankratz, Nathan organization: Department of Laboratory Medicine and Pathology, University of Minnesota School of Medicine, Minneapolis, Minnesota – sequence: 11 givenname: Dan E surname: Arking fullname: Arking, Dan E organization: McKusick-Nathans Institute of Genetic Medicine and Department of Medicine, Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, Maryland
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Snippet	Mitochondrial dysfunction in kidney cells has been implicated in the pathogenesis of CKD. Mitochondrial DNA (mtDNA) copy number is a surrogate measure of...
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SubjectTerms	Aged Atherosclerosis - complications DNA Copy Number Variations DNA, Mitochondrial - blood DNA, Mitochondrial - genetics Female Humans Male Middle Aged Prospective Studies Renal Insufficiency, Chronic - blood Renal Insufficiency, Chronic - epidemiology Renal Insufficiency, Chronic - etiology Risk Factors
Title	Association between Mitochondrial DNA Copy Number in Peripheral Blood and Incident CKD in the Atherosclerosis Risk in Communities Study
URI	https://www.ncbi.nlm.nih.gov/pubmed/26794963 https://www.proquest.com/docview/1807876895
Volume	27
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