Mitochondrial DNA copy number is associated with mortality and infections in a large cohort of patients with chronic kidney disease
Damage of mitochondrial DNA (mtDNA) with reduction in copy number has been proposed as a biomarker for mitochondrial dysfunction and oxidative stress. Chronic kidney disease (CKD) is associated with increased mortality and risk of cardiovascular disease, but the underlying mechanisms remain incomple...
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| Main Authors: | , , , , , , , , , , , , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
2019
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| In: |
Kidney international
Year: 2018, Volume: 96, Issue: 2, Pages: 480-488 |
| ISSN: | 1523-1755 |
| DOI: | 10.1016/j.kint.2019.04.021 |
| Online Access: | Verlag, Volltext: https://doi.org/10.1016/j.kint.2019.04.021 Verlag, Volltext: http://www.sciencedirect.com/science/article/pii/S0085253819304831 
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| Author Notes: | Federica Fazzini, Claudia Lamina, Liane Fendt, Ulla T. Schultheiss, Fruzsina Kotsis, Andrew A. Hicks, Heike Meiselbach, Hansi Weissensteiner, Lukas Forer, Vera Krane, Kai-Uwe Eckardt, Anna Köttgen and Florian Kronenberg; and the GCKD Investigators |
MARC
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| 500 | |a Current GCKD investigators and collaborators with the GCKD study are as follows: University of Erlangen-Nürnberg: Kai-Uwe Eckardt, Heike Meiselbach, Markus Schneider, Thomas Dienemann, Hans-Ulrich Prokosch, Barbara Bärthlein, Andreas Beck, Thomas Ganslandt, André Reis, Arif B. Ekici, Susanne Avendaño, Dinah Becker-Grosspitsch, Ulrike Alberth-Schmidt, Birgit Hausknecht, Rita Zitzmann, and Anke Weigel; University of Freiburg: Gerd Walz, Anna Köttgen, Ulla Schultheiß, Fruzsina Kotsis, Simone Meder, Erna Mitsch, and Ursula Reinhard; RWTH Aachen University: Jürgen Floege, Georg Schlieper,Turgay Saritas, Sabine Ernst, and Nicole Beaujean; Charité, University Medicine Berlin: Elke Schaeffner, Seema Baid-Agrawal, and Kerstin Theisen; Hannover Medical School: Hermann Haller, Jan Menne; University of Heidelberg: Martin Zeier, Claudia Sommerer, and Rebecca Woitke; University of Jena: Gunter Wolf, Martin Busch, and Rainer Fuß; Ludwig-Maximilians University of München: Thomas Sitter and Claudia Blank; University of Würzburg: Christoph Wanner, Vera Krane, Antje Börner-Klein, and Britta Bauer; Medical University of Innsbruck, Division of Genetic Epidemiology: Florian Kronenberg, Julia Raschenberger, Barbara Kollerits, Lukas Forer, Sebastian Schönherr, and Hansi Weissensteiner; University of Regensburg, Institute of Functional Genomics: Peter Oefner, Wolfram Gronwald, and Helena Zacharias; University Hospital of Bonn, Department of Medical Biometry, Informatics and Epidemiology (IMBIE): Matthias Schmid and Jennifer Nadal | ||
| 500 | |a Gesehen am 27.01.2020 | ||
| 500 | |a Received 12 December 2018 | ||
| 520 | |a Damage of mitochondrial DNA (mtDNA) with reduction in copy number has been proposed as a biomarker for mitochondrial dysfunction and oxidative stress. Chronic kidney disease (CKD) is associated with increased mortality and risk of cardiovascular disease, but the underlying mechanisms remain incompletely understood. Here we investigated the prognostic role of mtDNA copy number for cause-specific mortality in 4812 patients from the German Chronic Kidney Disease study, an ongoing prospective observational national cohort study of patients with CKD stage G3 and A1-3 or G1-2 with overt proteinuria (A3) at enrollment. MtDNA was quantified in whole blood using a plasmid-normalized PCR-based assay. At baseline, 1235 patients had prevalent cardiovascular disease. These patients had a significantly lower mtDNA copy number than patients without cardiovascular disease (fully-adjusted model: odds ratio 1.03, 95% confidence interval [CI] 1.01-1.05 per 10 mtDNA copies decrease). After four years of follow-up, we observed a significant inverse association between mtDNA copy number and all-cause mortality, adjusted for kidney function and cardiovascular disease risk factors (hazard ratio 1.37, 95% CI 1.09-1.73 for quartile 1 compared to quartiles 2-4). When grouped by causes of death, estimates pointed in the same direction for all causes but in a fully-adjusted model decreased copy numbers were significantly lower only in infection-related death (hazard ratio 1.82, 95% CI 1.08-3.08). A similar association was observed for hospitalizations due to infections in 644 patients (hazard ratio 1.19, 95% CI 1.00-1.42 in the fully-adjusted model). Thus, our data support a role of mitochondrial dysfunction in increased cardiovascular disease and mortality risks as well as susceptibility to infections in patients with CKD. | ||
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