Julia Raschenberger1, Barbara Kollerits1, Stephanie Titze2, Anna Köttgen3, Barbara Bärthlein4, Arif B Ekici5, Lukas Forer1, Sebastian Schönherr1, Hansi Weissensteiner1, Margot Haun1, Christoph Wanner6, Kai-Uwe Eckardt2, Florian Kronenberg7. 1. Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, Innsbruck, Austria. 2. Department of Nephrology and Hypertension, University of Erlangen-Nürnberg, Erlangen, Germany. 3. Division of Nephrology, Department of Medicine, University Medical Center Freiburg, Freiburg, Germany. 4. Chair of Medical Informatics, University of Erlangen-Nürnberg, Erlangen, Germany. 5. Institute of Human Genetics, University of Erlangen-Nürnberg, Erlangen, Germany. 6. Division of Nephrology, Department of Medicine, University of Würzburg, Würzburg, Germany. 7. Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, Innsbruck, Austria. Electronic address: Florian.Kronenberg@i-med.ac.at.
Abstract
BACKGROUND: Chronic kidney disease (CKD) affects 10-15% of the general population and affected individuals are at an increased risk for cardiovascular disease (CVD). Since telomere length is considered to be involved in biological aging, we tested whether relative telomere length (RTL) might be a marker for these two diseases. METHODS: The German Chronic Kidney Disease (GCKD) study is an ongoing prospective cohort study including patients with CKD of moderate severity. RTL was measured by qPCR in 4955 out of 5217 GCKD patients at baseline. RESULTS: RTL was distributed in the cohort with a mean ± SD of 0.95 ± 0.19. CVD was present in 1266 patients. Each decrease of RTL by 0.1 unit was associated with a higher probability for prevalent CVD: OR = 1.06, 95% CI 1.02-1.11, p = 0.007 (adjusted for age, sex, eGFR, BMI, ln-CRP, smoking, hypertension, diabetes, and lipids). Similar findings were observed for history of specific CVD entities, such as coronary artery disease (OR = 1.05, p = 0.025), myocardial infarction (OR = 1.08, p = 0.013) and percutaneous transluminal coronary angioplasty (OR = 1.06, p = 0.032). The strongest associations were found for interventions at the carotid arteries (OR = 1.25, p = 0.001) as well as aortic aneurysms (OR = 1.22, p = 0.001). CONCLUSIONS: In the presence of CKD there is a significant association between shorter RTL and CVD manifestations. RTL appears to be a marker reflecting changes in homeostasis associated with CKD that may contribute to the excess CVD risk.
BACKGROUND:Chronic kidney disease (CKD) affects 10-15% of the general population and affected individuals are at an increased risk for cardiovascular disease (CVD). Since telomere length is considered to be involved in biological aging, we tested whether relative telomere length (RTL) might be a marker for these two diseases. METHODS: The German Chronic Kidney Disease (GCKD) study is an ongoing prospective cohort study including patients with CKD of moderate severity. RTL was measured by qPCR in 4955 out of 5217 GCKD patients at baseline. RESULTS: RTL was distributed in the cohort with a mean ± SD of 0.95 ± 0.19. CVD was present in 1266 patients. Each decrease of RTL by 0.1 unit was associated with a higher probability for prevalent CVD: OR = 1.06, 95% CI 1.02-1.11, p = 0.007 (adjusted for age, sex, eGFR, BMI, ln-CRP, smoking, hypertension, diabetes, and lipids). Similar findings were observed for history of specific CVD entities, such as coronary artery disease (OR = 1.05, p = 0.025), myocardial infarction (OR = 1.08, p = 0.013) and percutaneous transluminal coronary angioplasty (OR = 1.06, p = 0.032). The strongest associations were found for interventions at the carotid arteries (OR = 1.25, p = 0.001) as well as aortic aneurysms (OR = 1.22, p = 0.001). CONCLUSIONS: In the presence of CKD there is a significant association between shorter RTL and CVD manifestations. RTL appears to be a marker reflecting changes in homeostasis associated with CKD that may contribute to the excess CVD risk.
Authors: Katarzyna Polonis; Virend K Somers; Christiane Becari; Naima Covassin; Phillip J Schulte; Brooke R Druliner; Ruth A Johnson; Krzysztof Narkiewicz; Lisa A Boardman; Prachi Singh Journal: Am J Physiol Heart Circ Physiol Date: 2017-08-19 Impact factor: 4.733
Authors: Are A Kalstad; Sjur Tveit; Peder L Myhre; Kristian Laake; Trine B Opstad; Arnljot Tveit; Erik B Schmidt; Svein Solheim; Harald Arnesen; Ingebjørg Seljeflot Journal: BMC Geriatr Date: 2019-12-27 Impact factor: 3.921