title: Is nonalbuminuric renal insufficiency in type 2 diabetes related to an increase in intrarenal vascular disease?
abstract: OBJECTIVE
  To investigate the role of intrarenal vascular disease in the pathogenesis of nonalbuminuric renal insufficiency in type 2 diabetes.
  
  
  METHODS
  We studied 325 unselected clinic patients who had sufficient clinical and biochemical information to calculate an estimated glomerular filtration rate (eGFR) using the Modified Diet in Renal Disease six-variable formula, at least two estimations of urinary albumin excretion rates (AER), and a renal duplex scan to estimate the resistance index of the interlobar renal arteries. The resistance index, measured as part of a complications surveillance program, was compared in patients with an eGFR < or >or=60 ml/min per 1.73 m(2) who were further stratified into normo- (AER <20), micro- (20-200), or macroalbuminuria (> 200 microg/min) categories.
  
  
  RESULTS
  Patients with an eGFR <60 ml/min per 1.73 m(2) had a higher resistance index of the renal interlobar arteries compared with patients with an eGFR >or=60 ml/min per 1.73 m(2). However, the resistance index was elevated to a similar extent in patients with an eGFR <60 ml/min per 1.73 m(2) regardless of albuminuric status (normo- 0.74 +/- 0.01, micro- 0.73 +/- 0.01, and macroalbuminuria resistance index 0.75 +/- 0.11). Multiple regression analysis revealed that increased age (P < 0.0001), elevated BMI (P = 0.0001), decreased eGFR (P < 0.01), and decreased diastolic blood pressure (P < 0.01), but not an increased AER, were independently associated with an elevated resistance index in patients with impaired renal function.
  
  
  CONCLUSIONS
  Subjects with type 2 diabetes and reduced glomerular filtration rate had similar degrees of intrarenal vascular disease, as measured by the intrarenal arterial resistance index, regardless of their AER status. The pathological mechanisms that determine the relationship between impaired renal function and AER status in subjects with type 2 diabetes remain to be elucidated.
authors.affiliation: Endocrine Centre and Department of Medicine, Austin Health, Heidelberg Repatriation Hospital, Waterdale Road, Heidelberg West, Victoria 3081, Australia. r.macisaac@unimelb.edu.au
authors.forename: Richard J
authors.initials: RJ
authors.lastname: MacIsaac
authors.forename: Sianna
authors.initials: S
authors.lastname: Panagiotopoulos
authors.forename: Karen J
authors.initials: KJ
authors.lastname: McNeil
authors.forename: Trudy J
authors.initials: TJ
authors.lastname: Smith
authors.forename: Con
authors.initials: C
authors.lastname: Tsalamandris
authors.forename: Huming
authors.initials: H
authors.lastname: Hao
authors.forename: P Geoffrey
authors.initials: PG
authors.lastname: Matthews
authors.forename: Merlin C
authors.initials: MC
authors.lastname: Thomas
authors.forename: David A
authors.initials: DA
authors.lastname: Power
authors.forename: George
authors.initials: G
authors.lastname: Jerums
mesh_terms: D000368:Aged; D000419:Albuminuria / Q000209:etiology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D003928:Diabetic Nephropathies / Q000000981:diagnostic imaging / Q000209:etiology / Q000652:urine*; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007676:Kidney Failure, Chronic / Q000209:etiology*; D008297:Male; D012077:Renal Artery / Q000000981:diagnostic imaging / Q000502:physiology; D014463:Ultrasonography; D014652:Vascular Diseases / Q000209:etiology