title: An immunohistochemical study of developing glomeruli in human fetal kidneys.
abstract: BACKGROUND
  In the glomerulonephritis, mesenchymal cells frequently repeat the expression of fetal immunohistochemical phenotypes. However, in human glomerulogenesis the phenotypic alteration of mesangial and other types of glomerular cells has not been clearly defined. Our aim was to clarify the characteristics of fetal mesangial cells and glomerular capillary endothelial cells, as well as their changes during glomerulogenesis using immunohistochemistry.
  
  
  METHODS
  We examined the renal tissues of 34 autopsied fetuses and neonates, 5 children, and 5 adults using immunohistochemistry and immunoelectron microscopy, using antibodies for cytoskeletons, contraction-associated proteins, and endothelial cell markers.
  
  
  RESULTS
  In the V and S stages, there were no cells showing mesangial and endothelial features within the vesicles and the S-shaped bodies. In the S stage, small blood vessels, consisting of endothelial cells (CD31+, CD34+) and primitive perivascular mesenchymal cells (alpha-smooth muscle actin+, low molecular caldesmon+, vimentin+), were branched from developing interlobular arteries and appeared to extend to the lower clefts of the S-shaped bodies. In the C stage, the perivascular mesenchymal cells aggregated at the root of the immature glomeruli. In the M stage, they migrated toward the periphery of immature glomeruli and gradually lost their fetal immunohistochemical features. Similarly, with further maturation, the fetal glomerular capillary endothelial cells gradually lost the immunostaining for CD34, while the strong staining intensity of CD31 remained unchanged, just as that in the adult glomerular capillary endothelial cells.
  
  
  CONCLUSIONS
  In human glomerulogenesis, we demonstrate that fetal mesangial and capillary endothelial cells change their immunohistochemical phenotypes with maturation. They gradually lose fetal immunohistochemical phenotypes. Already before birth, the mesangial cells in almost all glomeruli at the late M stage acquire the adult phenotype.
authors.affiliation: First Department of Pathology and Department of Pediatrics, Kochi Medical School, Kochi, Japan. chip@i-kochi.or.jp
authors.forename: K
authors.initials: K
authors.lastname: Naruse
authors.forename: M
authors.initials: M
authors.lastname: Fujieda
authors.forename: E
authors.initials: E
authors.lastname: Miyazaki
authors.forename: Y
authors.initials: Y
authors.lastname: Hayashi
authors.forename: M
authors.initials: M
authors.lastname: Toi
authors.forename: T
authors.initials: T
authors.lastname: Fukui
authors.forename: N
authors.initials: N
authors.lastname: Kuroda
authors.forename: M
authors.initials: M
authors.lastname: Hiroi
authors.forename: T
authors.initials: T
authors.lastname: Kurashige
authors.forename: H
authors.initials: H
authors.lastname: Enzan
mesh_terms: D000293:Adolescent; D000328:Adult; D002648:Child; D002675:Child, Preschool; D004730:Endothelium, Vascular / Q000196:embryology / Q000648:ultrastructure; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D007231:Infant, Newborn; D007678:Kidney Glomerulus / Q000098:blood supply / Q000196:embryology* / Q000648:ultrastructure; D008854:Microscopy, Electron; D016253:Microscopy, Immunoelectron; D011247:Pregnancy