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@ARTICLE{Sulaj:124294,
      author       = {A. Sulaj and S. Kopf and E. Gröne$^*$ and H.-J. Gröne$^*$
                      and S. Hoffmann and E. Schleicher and H.-U. Häring and V.
                      Schwenger and S. Herzig$^*$ and T. Fleming and P. P. Nawroth
                      and R. von Bauer},
      title        = {{ALCAM} a novel biomarker in patients with type 2 diabetes
                      mellitus complicated with diabetic nephropathy.},
      journal      = {Journal of diabetes and its complications},
      volume       = {31},
      number       = {6},
      issn         = {1056-8727},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DKFZ-2017-01190},
      pages        = {1058 - 1065},
      year         = {2017},
      abstract     = {Activated leukocyte cell adhesion molecule (ALCAM/CD166)
                      functions analogue to the receptor of advanced glycation end
                      products, which has been implicated in the development of
                      diabetic nephropathy (DN). We investigated the expression of
                      ALCAM and its ligand S100B in patients with DN.A total of 34
                      non-diabetic patients, 29 patients with type 2 diabetes and
                      normal albuminuria and 107 patients with type 2 diabetes
                      complicated with DN were assessed for serum concentration of
                      soluble ALCAM (sALCAM) by ELISA. Expression of ALCAM and
                      S100B in kidney histology from patients with DN was
                      determined by immunohistochemistry. Cell expression of ALCAM
                      and S100B was analyzed through confocal immunofluorescence
                      microscopy.Serum concentration of sALCAM was increased in
                      diabetic patients with DN compared to non-diabetic
                      (59.85±14.99ng/ml vs. 126.88±66.45ng/ml, P<0.0001).
                      Moreover sALCAM correlated positively with HbA1c (R=0.31,
                      P<0.0001), as well as with the stages of chronic kidney
                      disease and negatively correlated with eGFR (R=-0.20,
                      P<0.05). In diabetic patients with normal albuminuria sALCAM
                      was increased compared to patients with DN
                      (126.88±66.45ng/ml vs. 197.50±37.17ng/ml, P<0.0001). In
                      diabetic patients, ALCAM expression was significantly
                      upregulated in both the glomeruli and tubules (P<0.001).
                      ALCAM expression in the glomeruli correlated with presence
                      of sclerosis (R=0.25, P<0.001) and localized mainly in the
                      podocytes supporting the hypothesis that membrane bound
                      ALCAM drives diabetic nephropathy and thus explaining sALCAM
                      decrease in diabetic patients with DN. The expression of
                      S100B was increased significantly in the glomeruli of
                      diabetic patients (P<0.001), but not in the tubules. S100B
                      was as well localized in the podocytes.This study identifies
                      for the first time ALCAM as a potential mediator in the late
                      complications of diabetes in the kidney.},
      cin          = {G130},
      ddc          = {610},
      cid          = {I:(DE-He78)G130-20160331},
      pnm          = {322 - Genetics and Pathophysiology (POF3-322)},
      pid          = {G:(DE-HGF)POF3-322},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28325697},
      doi          = {10.1016/j.jdiacomp.2017.01.002},
      url          = {https://inrepo02.dkfz.de/record/124294},
}