title: Persistent arterial stiffness and endothelial dysfunction following successful pancreas-kidney transplantation in Type 1 diabetes.
abstract: OBJECTIVE
  Successful simultaneous pancreas-kidney transplantation (SPK) in Type 1 diabetic (T1DM) patients results in improved cardiovascular outcome and survival. However, it is doubtful whether the impairment of cardiovascular and endothelial function in T1DM can be completely reversed.
  
  
  METHODS
  Pulse-wave velocity, stroke volume, heart rate, serological markers of endothelial dysfunction (soluble intercellular, vascular cell-adhesion molecules, E-selectin, and plasminogen-activator-inhibitor-1) were measured in 10 T1DM patients after SPK with non-diabetic glucose levels, 10 T1DM patients with poor [T1DM>8; glycated haemoglobin (HbA1c)>8%], and 10 with good glucose control (T1DM<7, HbA1c<7%), in 6 non-diabetic patients after kidney transplantation (KT) and 9 non-diabetic control subjects (CON), matching for major anthropometric characteristics.
  
  
  RESULTS
  Pulse-wave velocity was increased in SPK (P < 0.02 vs. CON, KT, T1DM<7) and in T1DM>8 (P < 0.02 vs. T1DM<7). Systolic blood pressure was increased in SPK (P < 0.05 vs. CON). Stroke volume was reduced in SPK, T1DM>8 and T1DM<7 and KT (P < 0.01 vs. CON). Heart rate was elevated in SPK and in T1DM>8 (P < 0.0003 vs. CON and T1DM<7). In SPK, soluble intercellular and vascular cell-adhesion molecules were 100% and 44% higher (P < 0.03 vs. CON), respectively, while plasminogen-activator-inhibitor-1 was decreased in SPK (P < 0.02 vs. CON).
  
  
  CONCLUSIONS
  T1DM patients after SPK experience arterial stiffness, a higher heart-rate and blood pressure, reduced stroke volume and serological signs of endothelial dysfunction. Thus, functional and structural cardiovascular alterations as a result of glucotoxicity, uraemia and hypertension in T1DM might not be completely resolved by SPK.
authors.affiliation: 3rd Medical Department of Metabolic Diseases and Nephrology, Hietzing Hospital, A-1130 Vienna, Austria. marietta.stadler@wienkav.at
authors.forename: M
authors.initials: M
authors.lastname: Stadler
authors.forename: E
authors.initials: E
authors.lastname: Theuer
authors.forename: C
authors.initials: C
authors.lastname: Anderwald
authors.forename: U
authors.initials: U
authors.lastname: Hanusch-Enserer
authors.forename: M
authors.initials: M
authors.lastname: Auinger
authors.forename: C
authors.initials: C
authors.lastname: Bieglmayer
authors.forename: P
authors.initials: P
authors.lastname: Quehenberger
authors.forename: M
authors.initials: M
authors.lastname: Bischof
authors.forename: T
authors.initials: T
authors.lastname: Kästenbauer
authors.forename: M
authors.initials: M
authors.lastname: Wolzt
authors.forename: O
authors.initials: O
authors.lastname: Wagner
authors.forename: R
authors.initials: R
authors.lastname: Prager
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D050197:Atherosclerosis / Q000503:physiopathology*; D001783:Blood Flow Velocity / Q000502:physiology; D016022:Case-Control Studies; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology* / Q000601:surgery; D003925:Diabetic Angiopathies / Q000503:physiopathology*; D019040:E-Selectin / Q000097:blood; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D016035:Pancreas Transplantation; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D013318:Stroke Volume / Q000502:physiology; D016896:Treatment Outcome; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D055815:Young Adult
chemical_list: D019040:E-Selectin; D017395:Plasminogen Activator Inhibitor 1; D019010:Vascular Cell Adhesion Molecule-1