@article{FazziniLaminaFendtetal.2019,
  author    = {Fazzini, Federica and Lamina, Claudia and Fendt, Liane and Schultheiss, Ulla T. and Kotsis, Fruzsina and Hicks, Andrew A. and Meiselbach, Heike and Weissensteiner, Hansi and Forer, Lukas and Krane, Vera and Eckardt, Kai-Uwe and K{\"o}ttgen, Anna and Kronenberg, Florian},
  title     = {Mitochondrial DNA copy number is associated with mortality and infections in a large cohort of patients with chronic kidney disease},
  series = {Kidney International},
  volume    = {96},
  journal   = {Kidney International},
  organization    = {GCKD Investigators},
  doi       = {10.1016/j.kint.2019.04.021},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-227662},
  pages     = {480-488},
  year      = {2019},
  abstract  = {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.},
  language  = {en}
}
@article{MacdougallBircherEckhardtetal.2016,
  author    = {Macdougall, Iain C. and Bircher, Andreas J. and Eckhardt, Kai-Uwe and Obrador, Gregorio T. and Pollock, Carol A. and Stenvinkel, Peter and Swinkels, Dorine W. and Wanner, Christoph and Weiss, G{\"u}nter and Chertow, Glenn M.},
  title     = {Iron management in chronic kidney disease: conclusions from a "Kidney Disease: Improving Global Outcomes" (KDIGO) Controversies Conference},
  series = {Kidney International},
  volume    = {89},
  journal   = {Kidney International},
  number    = {1},
  doi       = {10.1016/j.kint.2015.10.002},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-191467},
  pages     = {28-39},
  year      = {2016},
  abstract  = {Before the introduction of erythropoiesis-stimulating agents (ESAs) in 1989, repeated transfusions given to patients with end-stage renal disease caused iron overload, and the need for supplemental iron was rare. However, with the widespread introduction of ESAs, it was recognized that supplemental iron was necessary to optimize hemoglobin response and allow reduction of the ESA dose for economic reasons and recent concerns about ESA safety. Iron supplementation was also found to be more efficacious via intravenous compared to oral administration, and the use of intravenous iron has escalated in recent years. The safety of various iron compounds has been of theoretical concern due to their potential to induce iron overload, oxidative stress, hypersensitivity reactions, and a permissive environment for infectious processes. Therefore, an expert group was convened to assess the benefits and risks of parenteral iron, and to provide strategies for its optimal use while mitigating the risk for acute reactions and other adverse effects.},
  language  = {en}
}