title: Correlation of autophagy type in podocytes with histopathological diagnosis of IgA nephropathy.
abstract: OBJECTIVE
  IgA nephropathy (IgA-N) frequently leads to progressive renal failure, thus estimation of the degree of progression is important for patient management. Autophagy is a mechanism that facilitates clearance of waste products to preserve renal function. The aim of this study was to assess autophagy in podocytes in children with progressive IgA-N at initial diagnosis by electron microscopy and investigate the relationship between the types of autophagy and severity of the disease.
  
  
  METHODS
  Renal biopsies from 16 children with established progressive IgA-N were examined by light and transmission electron microscopy with reference to autophagy types in the podocytes and histopathological diagnosis of IgA-N.
  
  
  RESULTS
  Two autophagy types were found. Type I rarely transformed to autophagic vacuoles and did not dissolve, thus possibly impairing cell function. However, type II frequently transformed to autophagosomes and autophagic vacuoles thus facilitating protein and lipid clearance. Of the 16 children studied, 8 (50%) with type I autophagy at initial diagnosis showed focal proliferative glomerulosclerosis (GN) of mild type (3 cases, 37.5%), mild/moderate type (2 cases, 25%) and moderate type (3 cases, 37.5%). In contrast, the remaining 8 children with type II autophagy at initial diagnosis showed focal proliferative GN of mild type in 7 (87.5%) and mild/moderate type in 1 (12.5%) case.
  
  
  CONCLUSIONS
  In IgA-N children, the occurrence of type I autophagy is correlated with histopathologically more progressive disease, possibly reflecting a tendency to a poorer prognosis.
authors.affiliation: Central Institute for Electron Microscopic Research, Nippon Medical School, Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Sato
authors.forename: T
authors.initials: T
authors.lastname: Yanagihara
authors.forename: M
authors.initials: M
authors.lastname: Ghazizadeh
authors.forename: M
authors.initials: M
authors.lastname: Ishizaki
authors.forename: A
authors.initials: A
authors.lastname: Adachi
authors.forename: Y
authors.initials: Y
authors.lastname: Sasaki
authors.forename: T
authors.initials: T
authors.lastname: Igarashi
authors.forename: Y
authors.initials: Y
authors.lastname: Fukunaga
mesh_terms: D000293:Adolescent; D001343:Autophagy / Q000502:physiology*; D002648:Child; D005260:Female; D005922:Glomerulonephritis, IGA / Q000473:pathology*; D006801:Humans; D008297:Male; D046529:Microscopy, Electron, Transmission; D050199:Podocytes / Q000648:ultrastructure*