title: Association between intrarenal arterial resistance and diastolic dysfunction in type 2 diabetes.
abstract: BACKGROUND
  In comparison to the well established changes in compliance that occur at the large vessel level in diabetes, much less is known about the changes in compliance of the cardiovascular system at the end-organ level. The aim of this study was therefore to examine whether there was a correlation between resistance of the intrarenal arteries of the kidney and compliance of the left ventricle, as estimated by measurements of diastolic function, in subjects with type 2 diabetes.
  
  
  METHODS
  We studied 167 unselected clinic patients with type 2 diabetes with a kidney duplex scan to estimate intrarenal vascular resistance, i.e. the resistance index (RI = peak systolic velocity-minimum diastolic velocity/peak systolic velocity) and a transthoracic echocardiogram (TTE) employing tissue doppler studies to document diastolic and systolic ventricular function.
  
  
  RESULTS
  Renal RI was significantly higher in subjects with diastolic dysfunction (0.72 +/- 0.05) when compared with those who had a normal TTE examination (0.66 +/- 0.06, p < 0.01). Renal RI values were correlated with markers of diastolic dysfunction including the E/Vp ratio (r = 0.41, p < 0.001), left atrial area (r = 0.36, p < 0.001), the E/A ratio (r = 0.36, p < 0.001) and the E/E' ratio (r = 0.31, p < 0.001). These associations were independent of systolic function, hypertension, the presence and severity of chronic kidney disease, the use of renin-angiotensin inhibitors and other potentially confounding variables.
  
  
  CONCLUSIONS
  Increasing vascular resistance of the intrarenal arteries was associated with markers of diastolic dysfunction in subjects with type 2 diabetes. These findings are consistent with the hypothesis that vascular and cardiac stiffening in diabetes are manifestations of common pathophysiological mechanisms.
authors.affiliation: Endocrine Centre, Austin Health & University of Melbourne, Melbourne, Australia. r.macisaac@unimelb.edu.au
authors.forename: Richard J
authors.initials: RJ
authors.lastname: MacIsaac
authors.forename: Merlin C
authors.initials: MC
authors.lastname: Thomas
authors.forename: Sianna
authors.initials: S
authors.lastname: Panagiotopoulos
authors.forename: Trudy J
authors.initials: TJ
authors.lastname: Smith
authors.forename: Huming
authors.initials: H
authors.lastname: Hao
authors.forename: D Geoffrey
authors.initials: DG
authors.lastname: Matthews
authors.forename: George
authors.initials: G
authors.lastname: Jerums
authors.forename: Louise M
authors.initials: LM
authors.lastname: Burrell
authors.forename: Piyush M
authors.initials: PM
authors.lastname: Srivastava
mesh_terms: D000328:Adult; D000368:Aged; D003187:Compliance; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000503:physiopathology*; D003971:Diastole / Q000502:physiology*; D004452:Echocardiography; D005260:Female; D006801:Humans; D007668:Kidney / Q000098:blood supply; D008297:Male; D008875:Middle Aged; D012077:Renal Artery / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology*; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology*