title: Renal structure in normoalbuminuric and albuminuric patients with type 2 diabetes and impaired renal function.
abstract: OBJECTIVE
  The structural basis of normoalbuminuric renal insufficiency in patients with type 2 diabetes remains to be elucidated. We compared renal biopsy findings in patients with type 2 diabetes and estimated glomerular filtration rate (eGFR) and measured GFR of <60 mL/min/1.73 m2, associated with either normo-, micro-, or macroalbuminuria.
  
  
  METHODS
  In patients with normo- (n = 8) or microalbuminuria (n = 6), renal biopsies were performed according to a research protocol. In patients with macroalbuminuria (n = 17), biopsies were performed according to clinical indication. Findings were categorized according to the Fioretto classification: category 1 (C1), normal/near normal; category 2 (C2), typical diabetic nephropathy (DN) with predominantly glomerular changes; and category 3 (C3), atypical with disproportionately severe interstitial/tubular/vascular damage and with no/mild diabetic glomerular changes.
  
  
  RESULTS
  In our study population (mean eGFR 35 mL/min/1.73 m2), typical glomerular changes (C2) of DN were observed in 22 of 23 subjects with micro- or macroalbuminuria compared with 3 of 8 subjects with normoalbuminuria (P = 0.002). By contrast, predominantly interstitial or vascular changes (C3) were seen in only 1 of 23 subjects with micro- or macroalbuminuria compared with 3 of 8 normoalbuminuric subjects (P = 0.08). Mesangial area increased progressively from normal controls to patients with type 2 diabetes and normo-, micro-, and macroalbuminuria. Varying degrees of arteriosclerosis, although not necessarily the predominant pattern, were seen in seven of eight subjects with normoalbuminuria.
  
  
  CONCLUSIONS
  Typical renal structural changes of DN were observed in patients with type 2 diabetes and elevated albuminuria. By contrast, in normoalbuminuric renal insufficiency, these changes were seen less frequently, likely reflecting greater contributions from aging, hypertension, and arteriosclerosis.
authors.affiliation: Corresponding author: Elif I. Ekinci, elif.ekinci@unimelb.edu.au.
authors.forename: Elif I
authors.initials: EI
authors.lastname: Ekinci
authors.forename: George
authors.initials: G
authors.lastname: Jerums
authors.forename: Alison
authors.initials: A
authors.lastname: Skene
authors.forename: Paul
authors.initials: P
authors.lastname: Crammer
authors.forename: David
authors.initials: D
authors.lastname: Power
authors.forename: Karey Y
authors.initials: KY
authors.lastname: Cheong
authors.forename: Sianna
authors.initials: S
authors.lastname: Panagiotopoulos
authors.forename: Karen
authors.initials: K
authors.lastname: McNeil
authors.forename: Scott T
authors.initials: ST
authors.lastname: Baker
authors.forename: Paola
authors.initials: P
authors.lastname: Fioretto
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Macisaac
mesh_terms: D000368:Aged; D000419:Albuminuria / Q000209:etiology / Q000473:pathology*; D001706:Biopsy; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000473:pathology*; D003928:Diabetic Nephropathies / Q000209:etiology / Q000473:pathology*; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007678:Kidney Glomerulus / Q000473:pathology*; D008297:Male; D051437:Renal Insufficiency / Q000209:etiology / Q000473:pathology*