title: GSTT1 gene abnormality in minimal change nephrotic syndrome with elevated serum immunoglobulin E.
abstract: BACKGROUND
  Imbalance between T-helper 1 (Th1) and 2 (Th2) lymphocytes and effects of reactive oxygen species (ROS) upon glomerular capillary walls have been implicated in minimal change nephrotic syndrome (MCNS).
  
  
  METHODS
  By polymerase chain reaction and comparative genomic hybridization, we evaluated mutations of the GSTT1 gene (GSTT1), a member of the glutathione S-transferase (GST) supergene family associated with both protection of cells from ROS and control of allergic reactions and serum immunoglobulin (Ig) E.
  
  
  RESULTS
  Among 15 children with MCNS, IgE elevation (over 2,000 IU/l) and GSTT1 deletion was found in 2 who showed severe allergic symptoms. Serum ROS concentrations in these 2 patients were significantly higher than in healthy controls or other MCNS patients. In addition, a Th2 shift caused by increased serum interleukin (IL)- 4 was observed.
  
  
  CONCLUSIONS
  These results suggest presence of a GSTT1 abnormality in some children with MCNS having marked serum IgE elevations and various allergic complications. Defective ROS degradation and Th1/Th2 imbalance caused by GSTT1 abnormality could initiate proteinuria leading to MCNS.
authors.affiliation: Department of Pediatrics, Kinki University School of Medicine, Osaka, Japan.
authors.forename: Kohei
authors.initials: K
authors.lastname: Miyazaki
authors.forename: Keisuke
authors.initials: K
authors.lastname: Sugimoto
authors.forename: Shoji
authors.initials: S
authors.lastname: Tsuji
authors.forename: Anna
authors.initials: A
authors.lastname: Iharada
authors.forename: Shinsuke
authors.initials: S
authors.lastname: Fujita
authors.forename: Hidehiko
authors.initials: H
authors.lastname: Yanagida
authors.forename: Naoki
authors.initials: N
authors.lastname: Sakata
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Okada
authors.forename: Kazunari
authors.initials: K
authors.lastname: Kaneko
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Takemura
mesh_terms: D000293:Adolescent; D015415:Biomarkers / Q000097:blood; D001706:Biopsy; D002648:Child; D055028:Comparative Genomic Hybridization; D003520:Cyclophosphamide / Q000627:therapeutic use; D016572:Cyclosporine / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005500:Follow-Up Studies; D005982:Glutathione Transferase / Q000235:genetics*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood*; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008297:Male; D009154:Mutation; D009402:Nephrosis, Lipoid / Q000097:blood / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D016133:Polymerase Chain Reaction; D011507:Proteinuria / Q000150:complications / Q000209:etiology; D017382:Reactive Oxygen Species / Q000097:blood / Q000378:metabolism*; D012263:Ribonucleosides / Q000627:therapeutic use; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D007166:Immunosuppressive Agents; D017382:Reactive Oxygen Species; D012263:Ribonucleosides; D007073:Immunoglobulin E; C010052:mizoribine; D016572:Cyclosporine; D003520:Cyclophosphamide; C413545:glutathione S-transferase T1; D005982:Glutathione Transferase