title: Improvement of kidney failure with fetal kidney precursor cell transplantation.
abstract: BACKGROUND
  Current therapies for end-stage renal disease have severe limitations. Dialysis is only a temporary treatment and does not restore kidney function. Transplantation is limited by donor organ shortage and immune-related problems. Here, we show that the transplantation of fetal kidney precursor cells reconstitutes kidney tissues, reduces uremic symptoms, and provides life-saving metabolic support in kidney failure animal models.
  
  
  METHODS
  Kidney failure was surgically induced by resecting kidneys, leaving approximately 1/6 of the total kidney mass (5/6 nephrectomy). Fetal kidney precursor cells were isolated from metanephroi of E17.5 rat fetuses using collagenase/dispase digestion. Five weeks after the nephrectomy procedure, isolated fetal kidney precursor cells were transplanted under the kidney capsule of rats using fibrin gel matrix. Six and ten weeks after transplantation, animals were analyzed biochemically and the grafts were retrieved for histological analyses.
  
  
  RESULTS
  Five weeks after the nephrectomy, glomerular hypertrophy, and increased blood urea nitrogen and serum creatinine levels were observed. The cell transplantation into the kidneys of kidney failure-induced rats resulted in kidney tissue reconstitution and the transplanted cells were observed in the reconstitution region of the kidneys as evidenced by the presence of fluorescently labeled cells. In addition, biochemical parameters from serum and urine samples showed improved kidney functions compared with non-treated group without severe immune response after ten weeks.
  
  
  CONCLUSIONS
  Transplanting fetal kidney precursor cells showed the potential for the partial augmentation of kidney structure and function in the treatment of kidney failure.
authors.affiliation: Department of Bioengineering, Hanyang University, Seoul, Korea.
authors.forename: Sang-Soo
authors.initials: SS
authors.lastname: Kim
authors.forename: Heung Jae
authors.initials: HJ
authors.lastname: Park
authors.forename: Joungho
authors.initials: J
authors.lastname: Han
authors.forename: So-Jung
authors.initials: SJ
authors.lastname: Gwak
authors.forename: Moon Hyang
authors.initials: MH
authors.lastname: Park
authors.forename: Kang Won
authors.initials: KW
authors.lastname: Song
authors.forename: Yun Hee
authors.initials: YH
authors.lastname: Rhee
authors.forename: Hyung
authors.initials: H
authors.lastname: Min Chung
authors.forename: Byung-Soo
authors.initials: BS
authors.lastname: Kim
mesh_terms: D000818:Animals; D002462:Cell Membrane; D004195:Disease Models, Animal; D018450:Disease Progression; D004198:Disease Susceptibility; D053595:Embryonic Stem Cells / Q000637:transplantation*; D005923:Glomerulosclerosis, Focal Segmental / Q000473:pathology / Q000503:physiopathology; D006084:Graft Rejection / Q000209:etiology; D006984:Hypertrophy; D007668:Kidney / Q000473:pathology / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000473:pathology / Q000503:physiopathology; D009392:Nephrectomy; D010641:Phenotype; D051381:Rats; D017207:Rats, Sprague-Dawley; D012038:Regeneration; D051437:Renal Insufficiency / Q000150:complications / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery*; D016019:Survival Analysis; D014511:Uremia / Q000503:physiopathology