title: The urinary podocyte as a marker for the differential diagnosis of idiopathic focal glomerulosclerosis and minimal-change nephrotic syndrome.
abstract: OBJECTIVE
  Detection of podocytes in the urine sediment of children indicates that severe podocyte injury occurred in the glomerulus. Focal glomerulosclerosis (FGS) and minimal-change nephrotic syndrome (MCNS) are kidney diseases characterized by massive proteinuria. The aim of the present study was to determine whether urinary podocytes can be detected in patients with idiopathic FGS or MCNS and whether immunosuppression therapy alters these cells.
  
  
  METHODS
  Twenty patients with MCNS (nephrotic stage, n = 12; remission stage, n = 8), 15 patients with FGS and 20 healthy controls were included in the present study. Urinary podocytes were stained by immunofluorescence. All patients with MCNS at the nephrotic stage received prednisolone for 6 months, and all patients with FGS received some form of immunosuppression therapy including prednisolone, cyclophosphamide or mizoribine for 12 months.
  
  
  RESULTS
  The 12 nephrotic-stage MCNS patients achieved remission after treatment. Seven of the 15 FGS patients also achieved remission, but the other 8 remained in the nephrotic stage. Urinary podocytes were not detected in any patient with MCNS nor were they detected in healthy controls. Urinary podocytes were detected in all FGS patients (mean, 4.2 cells/ml) before treatment and the number of cells decreased in the 7 patients who achieved remission. The number of podocytes was unchanged in the other 8 patients even after treatment.
  
  
  CONCLUSIONS
  Urinary podocytes may be a useful diagnostic indicator for differentiation between FGS and MCNS. These cells may also mark disease progression in cases of FGS.
authors.affiliation: Department of Medicine, Misato Junshin Hospital, Saitama, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: C
authors.initials: C
authors.lastname: Ushiyama
authors.forename: S
authors.initials: S
authors.lastname: Suzuki
authors.forename: M
authors.initials: M
authors.lastname: Hara
authors.forename: N
authors.initials: N
authors.lastname: Shimada
authors.forename: I
authors.initials: I
authors.lastname: Ebihara
authors.forename: H
authors.initials: H
authors.lastname: Koide
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D015415:Biomarkers / Q000652:urine; D016022:Case-Control Studies; D003520:Cyclophosphamide / Q000627:therapeutic use; D003937:Diagnosis, Differential; D018450:Disease Progression; D005260:Female; D005455:Fluorescent Antibody Technique; D005923:Glomerulosclerosis, Focal Segmental / Q000175:diagnosis* / Q000188:drug therapy / Q000652:urine; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008297:Male; D009402:Nephrosis, Lipoid / Q000175:diagnosis* / Q000188:drug therapy / Q000652:urine; D011239:Prednisolone / Q000627:therapeutic use; D011507:Proteinuria; D012263:Ribonucleosides / Q000627:therapeutic use; D018709:Statistics, Nonparametric; D016896:Treatment Outcome; D014556:Urine / Q000166:cytology*
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D007166:Immunosuppressive Agents; D012263:Ribonucleosides; C010052:mizoribine; D003520:Cyclophosphamide; D011239:Prednisolone