title: Soluble CD25 is increased in patients with sepsis-induced acute kidney injury.
abstract: OBJECTIVE
  Sepsis has been shown to induce the expansion of CD4+CD25+ regulatory T cells (Tregs), and this paradoxical immune suppression has been suggested to be closely associated with the development of sepsis-induced organ dysfunction. In the present study, we aimed to investigate the possible link between immune suppression and the development of septic acute kidney injury (AKI).
  
  
  METHODS
  We prospectively enrolled patients with a diagnosis of sepsis, with or without AKI and as well as patients with AKI but without sepsis. Serum and urine samples at the time of the diagnosis were collected to measure neutrophil gelatinase-associated lipocalin (NGAL), cytokines, and soluble CD25 (sCD25).
  
  
  RESULTS
  Of the 82 patients enrolled, 44, 18, and 20 patients were classified into septic-AKI, sepsis-non AKI and non-septic AKI groups. There were no differences in the baseline characteristics in all three groups and the severity of infection in the two sepsis groups. Serum levels of interleukin (IL)-10 were significantly elevated in patients with septic-AKI compared to the other two groups. Serum and urine NGAL levels and the level of serum sCD25, a marker of regulatory T cells, were significantly elevated in patients with septic AKI group, indicating the potential association of paradoxical immune suppression and the development of septic-AKI.
  
  
  CONCLUSIONS
  These results suggest that immune suppression in sepsis may be closely linked to the development of AKI and that sCD25 or IL-10 may be useful as novel biomarkers for the development of septic AKI.
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
authors.forename: Eunjung
authors.initials: E
authors.lastname: Cho
authors.forename: Ji Hyun
authors.initials: JH
authors.lastname: Lee
authors.forename: Hye Jin
authors.initials: HJ
authors.lastname: Lim
authors.forename: Se Won
authors.initials: SW
authors.lastname: Oh
authors.forename: Sang Kyung
authors.initials: SK
authors.lastname: Jo
authors.forename: Won Yong
authors.initials: WY
authors.lastname: Cho
authors.forename: Houng-Kyu
authors.initials: HK
authors.lastname: Kim
authors.forename: So Young
authors.initials: SY
authors.lastname: Lee
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology* / Q000276:immunology / Q000378:metabolism*; D000209:Acute-Phase Proteins / Q000652:urine; D000368:Aged; D000369:Aged, 80 and over; D001424:Bacterial Infections / Q000150:complications / Q000276:immunology / Q000378:metabolism; D015415:Biomarkers / Q000097:blood / Q000652:urine; D005260:Female; D006801:Humans; D016753:Interleukin-10 / Q000097:blood / Q000276:immunology; D053645:Interleukin-2 Receptor alpha Subunit / Q000097:blood* / Q000276:immunology; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood / Q000652:urine; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011518:Proto-Oncogene Proteins / Q000097:blood / Q000652:urine; D018805:Sepsis / Q000150:complications* / Q000276:immunology / Q000378:metabolism*; D012995:Solubility; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism
chemical_list: D000209:Acute-Phase Proteins; D015415:Biomarkers; C508609:IL10 protein, human; C508017:IL2RA protein, human; D053645:Interleukin-2 Receptor alpha Subunit; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins; D016753:Interleukin-10
keywords: acute kidney injury; immune suppression; sepsis; soluble CD25