title: Kidney transplantation improves arterial function measured by pulse wave analysis and endothelium-independent dilatation in uraemic patients despite deterioration of glucose metabolism.
abstract: BACKGROUND
  The aim of this study is to investigate the effect of kidney transplantation on arterial function in relation to changes in glucose metabolism.
  
  
  METHODS
  Included were 40 kidney recipients (Tx group, age 38 ± 13 years) and 40 patients without known diabetes remaining on the waiting list for kidney transplantation (uraemic control group, age 47 ± 11 years). Arterial function was estimated by the pulse wave velocity (PWV) of the carotid-femoral pulse wave, aortic augmentation index (AIX), flow-mediated (FMD) and nitroglycerin-induced vasodilatation (NID) of the brachial artery performed before transplantation and after 12 months. PWV recorded sequentially at the carotid and femoral artery is an estimate of arterial stiffness; AIX is an integrated index of vascular and ventricular function. FMD and NID are the dilatory capacities of the brachial artery after increased flow (endothelium dependent) and after nitroglycerin administration (endothelium independent). The insulin resistance was estimated by the insulin sensitivity index (ISI).
  
  
  RESULTS
  AIX was reduced from 27% (17-33) to 14% (7-25) (P = 0.01) after 1 year in the Tx group and remained stable in uraemic controls (P = 0.001, between groups), and NID increased from 11% (7-16) to 18% (12-23) (P = 0.0005). At baseline, carotid-femoral PWV was similar in the Tx group, uraemic controls and healthy controls and it did not change significantly after transplantation. ISI deteriorated in the Tx group from 7.2 ± 4.0 to 5.0 ± 3.0 (P = 0.005) and remained stable in uraemic controls (7.9 ± 5.1 vs 8.5 ± 4.9, NS). Mean arterial blood pressure decreased from 105 ± 13 to 96 ± 11 mmHg (P = 0.005) in the Tx group despite a 20% lower use of antihypertensive agents.
  
  
  CONCLUSIONS
  Arterial function measured by AIX and NID was improved 1 year after kidney transplantation. This was associated with a decline in blood pressure and seen inspite of an increase in insulin resistance.
authors.affiliation: Department of Nephrology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. mads.hornum@rh.dk
authors.forename: Mads
authors.initials: M
authors.lastname: Hornum
authors.forename: Peter
authors.initials: P
authors.lastname: Clausen
authors.forename: Thomas
authors.initials: T
authors.lastname: Idorn
authors.forename: Jesper Melchior
authors.initials: JM
authors.lastname: Hansen
authors.forename: Elisabeth R
authors.initials: ER
authors.lastname: Mathiesen
authors.forename: Bo
authors.initials: B
authors.lastname: Feldt-Rasmussen
mesh_terms: D000328:Adult; D001158:Arteries / Q000503:physiopathology*; D001783:Blood Flow Velocity; D001794:Blood Pressure; D016022:Case-Control Studies; D004106:Dilatation; D004730:Endothelium, Vascular / Q000473:pathology*; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate; D005947:Glucose / Q000378:metabolism*; D005951:Glucose Tolerance Test; D006339:Heart Rate; D006801:Humans; D007333:Insulin Resistance; D007676:Kidney Failure, Chronic / Q000628:therapy; D007677:Kidney Function Tests; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D005996:Nitroglycerin / Q000633:toxicity; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors; D014511:Uremia / Q000503:physiopathology*; D014664:Vasodilation
chemical_list: D005996:Nitroglycerin; D005947:Glucose