title: Peripheral augmentation index and vascular inflammation in autosomal dominant polycystic kidney disease.
abstract: BACKGROUND
  Cardiovascular disease is the leading cause of premature mortality in autosomal dominant polycystic kidney disease (ADPKD). We examined peripheral augmentation index (AIx) as a measure of systemic vascular function and circulating markers of vascular inflammation in patients with ADPKD.
  
  
  METHODS
  Fifty-two ADPKD patients with hypertension and estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m(2), 50 ADPKD patients with hypertension and eGFR ≥ 60 mL/min/1.73 m(2), 42 normotensive ADPKD patients with eGFR ≥ 60 mL/min/1.73 m(2) and 51 normotensive healthy controls were enrolled in this study. AIx was measured from peripheral artery tone recordings using finger plethysmography. Serum levels of soluble intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule-1, P-selectin, E-selectin, soluble Fas (sFas) and Fas ligand (FasL) were measured as markers of vascular inflammation.
  
  
  RESULTS
  AIx was higher in all three patient groups with ADPKD compared to healthy controls (P < 0.05). AIx was similar between the normotensive ADPKD patients with eGFR ≥ 60 mL/min/1.73 m(2) and hypertensive ADPKD patients with eGFR < 60 mL/min/1.73 m(2) (P > 0.05). ICAM, P-selectin, E-selectin and sFas were higher and FasL lower in all ADPKD groups compared to controls (P < 0.05). ICAM, P-selectin and E-selectin were similar between the normotensive ADPKD patients with eGFR ≥ 60 mL/min/1.73 m(2) and hypertensive ADPKD patients with eGFR < 60 mL/min/1.73 m(2) (P > 0.05). According to multiple regression analysis, predictors of AIx in ADPKD included age, height, heart rate and mean arterial pressure (P < 0.05). Vascular inflammatory markers were not predictors of AIx in ADPKD.
  
  
  CONCLUSIONS
  Systemic vascular dysfunction, manifesting as an increase in AIx and vascular inflammation is evident in young normotensive ADPKD patients with preserved renal function. Vascular inflammation is not associated with elevated AIx in ADPKD.
authors.affiliation: Department of Epidemiology and Public Health, National University of Singapore. kheffernan@tuftsmedicalcetner.org
authors.forename: Kevin S
authors.initials: KS
authors.lastname: Heffernan
authors.forename: Jeffrey T
authors.initials: JT
authors.lastname: Kuvin
authors.forename: Mark J
authors.initials: MJ
authors.lastname: Sarnak
authors.forename: Ronald D
authors.initials: RD
authors.lastname: Perrone
authors.forename: Dana C
authors.initials: DC
authors.lastname: Miskulin
authors.forename: Darya
authors.initials: D
authors.lastname: Rudym
authors.forename: Priya
authors.initials: P
authors.lastname: Chandra
authors.forename: Richard H
authors.initials: RH
authors.lastname: Karas
authors.forename: Vandana
authors.initials: V
authors.lastname: Menon
mesh_terms: D000328:Adult; D001794:Blood Pressure; D016022:Case-Control Studies; D019040:E-Selectin / Q000378:metabolism; D005260:Female; D005919:Glomerular Filtration Rate; D006339:Heart Rate; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism; D007249:Inflammation / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000378:metabolism; D016891:Polycystic Kidney, Autosomal Dominant / Q000150:complications* / Q000378:metabolism; D011379:Prognosis; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D014652:Vascular Diseases / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism
chemical_list: D019040:E-Selectin; D019007:P-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1