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@ARTICLE{Russ:140946,
      author       = {Russ, Martin and Ott, Sascha and Bedarf, Janis R and
                      Kirschfink, Michael and Hiebl, Bernhard and Unger, Juliane
                      K},
      title        = {{I}ncreased compensatory kidney workload results in
                      cellular damage in a short time porcine model of mixed
                      acidemia - {I}s acidemia a 'first hit' in acute kidney
                      injury?},
      journal      = {PLOS ONE},
      volume       = {14},
      number       = {6},
      issn         = {1932-6203},
      address      = {San Francisco, California, US},
      publisher    = {PLOS},
      reportid     = {DZNE-2020-07268},
      pages        = {e0218308},
      year         = {2019},
      abstract     = {Acute kidney injury (AKI) corrupts the outcome of about
                      $50\%$ of all critically ill patients. We investigated the
                      possible contribution of the pathology acidemia on the
                      development of AKI. Pigs were exposed to acidemia, acidemia
                      plus hypoxemia or a normal acid-base balance in an
                      experimental setup, which included mechanical ventilation
                      and renal replacement therapy to facilitate biotrauma caused
                      by extracorporeal therapies. Interestingly, extensive
                      histomorphological changes like a tubular loss of cell
                      barriers occurred in the kidneys after just 5 hours exposure
                      to acidemia. The additional exposure to hypoxemia aggravated
                      these findings. These 'early' microscopic pathologies
                      opposed intra vitam data of kidney function. They did not
                      mirror cellular or systemic patterns of proinflammatory
                      molecules (like TNF-α or IL 18) nor were they detectable by
                      new, sensitive markers of AKI like Neutrophil
                      gelatinase-associated lipocalin. Instead, the data suggest
                      that the increased renal proton excretion during acidemia
                      could be an 'early' first hit in the multifactorial
                      pathogenesis of AKI.},
      keywords     = {Acid-Base Imbalance: complications / Acute Kidney Injury:
                      etiology / Animals / Hypoxia / Kidney: physiopathology /
                      Kidney Tubules: pathology / Protons / Swine},
      cin          = {AG Tamgüney 2},
      ddc          = {610},
      cid          = {I:(DE-2719)1013022},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31206554},
      pmc          = {pmc:PMC6576776},
      doi          = {10.1371/journal.pone.0218308},
      url          = {https://pub.dzne.de/record/140946},
}