title: Podocyte structural parameters do not predict progression to diabetic nephropathy in normoalbuminuric type 1 diabetic patients.
abstract: BACKGROUND
  Podocyte injury has been implicated in diabetic nephropathy (DN) ranging from normoalbuminuria to proteinuria in both type 1 and type 2 diabetes.
  
  
  METHODS
  To determine whether podocyte structural parameters predict DN risk in initially normoalbuminuric long-standing type 1 diabetic patients, we performed a nested case-control study in sex and diabetes duration-matched progressors (progression to proteinuria or ESRD, n = 10), non-progressors (normoalbuminuric at follow-up, n = 10), and non-diabetic controls (n = 10).
  
  
  RESULTS
  HbA1c and diastolic blood pressure were higher in progressors versus non-progressors. Podocyte number per glomerulus, numerical density of podocyte per glomerulus, and foot process width were not different among groups. The glomerular basement membrane width was greater in progressors versus non-progressors or controls, and in non-progressors versus controls. As expected, the mesangial fractional volume was greater in progressors and non-progressors versus controls, with no differences between progressors and non-progressors.
  
  
  CONCLUSIONS
  This study does not indicate that podocyte structural changes are preconditions for later DN progression in initially normoalbuminuric type 1 diabetic patients. However, this does not preclude an important role for podocyte injury at a later stage of DN.
authors.affiliation: Departmentsof Medicine, University of Minnesota, Minneapolis, Minn., USA.
authors.forename: Tasma
authors.initials: T
authors.lastname: Harindhanavudhi
authors.forename: Alicia
authors.initials: A
authors.lastname: Parks
authors.forename: Michael
authors.initials: M
authors.lastname: Mauer
authors.forename: M Luiza
authors.initials: ML
authors.lastname: Caramori
mesh_terms: D000328:Adult; D000419:Albuminuria / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D001794:Blood Pressure; D016022:Case-Control Studies; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000378:metabolism*; D003928:Diabetic Nephropathies / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D050533:Glomerular Basement Membrane / Q000473:pathology* / Q000648:ultrastructure; D005920:Glomerular Mesangium / Q000473:pathology* / Q000648:ultrastructure; D006442:Glycated Hemoglobin / Q000378:metabolism*; D006801:Humans; D008297:Male; D008854:Microscopy, Electron; D050199:Podocytes / Q000473:pathology* / Q000648:ultrastructure; D055815:Young Adult
chemical_list: D006442:Glycated Hemoglobin; C517652:hemoglobin A1c protein, human