@article{GalloWardFotheringhametal.2016,
  author    = {Gallo, Linda A. and Ward, Micheal S. and Fotheringham, Amelia K. and Zhuang, Aowen and Borg, Danielle J. and Flemming, Nicole B. and Harvie, Ben M. and Kinneally, Toni L. and Yeh, Shang-Ming and McCarthy, Domenica A. and Koepsell, Hermann and Vallon, Volker and Pollock, Carol and Panchapakesan, Usha and Forbes, Josephine M.},
  title     = {Once daily administration of the SGLT2 inhibitor, empagliflozin, attenuates markers of renal fibrosis without improving albuminuria in diabetic db/db mice},
  series = {Scientific Reports},
  volume    = {6},
  journal   = {Scientific Reports},
  number    = {26428},
  doi       = {10.1038/srep26428},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-167678},
  year      = {2016},
  abstract  = {Blood glucose control is the primary strategy to prevent complications in diabetes. At the onset of kidney disease, therapies that inhibit components of the renin angiotensin system (RAS) are also indicated, but these approaches are not wholly effective. Here, we show that once daily administration of the novel glucose lowering agent, empagliflozin, an SGLT2 inhibitor which targets the kidney to block glucose reabsorption, has the potential to improve kidney disease in type 2 diabetes. In male db/db mice, a 10-week treatment with empagliflozin attenuated the diabetes-induced upregulation of profibrotic gene markers, fibronectin and transforming-growth-factor-beta. Other molecular (collagen IV and connective tissue growth factor) and histological (tubulointerstitial total collagen and glomerular collagen IV accumulation) benefits were seen upon dual therapy with metformin. Albuminuria, urinary markers of tubule damage (kidney injury molecule-1, KIM-1 and neutrophil gelatinase-associated lipocalin, NGAL), kidney growth, and glomerulosclerosis, however, were not improved with empagliflozin or metformin, and plasma and intra-renal renin activity was enhanced with empagliflozin. In this model, blood glucose lowering with empagliflozin attenuated some molecular and histological markers of fibrosis but, as per treatment with metformin, did not provide complete renoprotection. Further research to refine the treatment regimen in type 2 diabetes and nephropathy is warranted.},
  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}
}