title: Intradialytic hypertension and its association with endothelial cell dysfunction.
abstract: OBJECTIVE
  Intradialytic hypertension is associated with adverse outcomes, yet the mechanism is uncertain. Patients with intradialytic hypertension exhibit imbalances in endothelial-derived vasoregulators nitric oxide and endothelin-1, indirectly suggesting endothelial cell dysfunction. We hypothesized that intradialytic hypertension is associated in vivo with endothelial cell dysfunction, a novel predictor of adverse cardiovascular outcomes.
  
  
  METHODS
  We performed a case-control cohort study including 25 hemodialysis (HD) subjects without (controls) and 25 with intradialytic hypertension (an increase in systolic BP pre- to postdialysis ≥10 mmHg ≥4/6 consecutive HD sessions). The primary outcome was peripheral blood endothelial progenitor cells (EPCs) assessed by aldehyde dehydrogenase activity (ALDH(br)) and cell surface marker expression (CD34(+)CD133(+)). We also assessed endothelial function by ultrasonographic measurement of brachial artery flow-mediated vasodilation (FMD) normalized for shear stress. Parametric and nonparametric t tests were used to compare EPCs, FMD, and BP.
  
  
  RESULTS
  Baseline characteristics and comorbidities were similar between groups. Compared with controls, 2-week average predialysis systolic BP was lower among subjects with intradialytic hypertension (144.0 versus 155.5 mmHg), but postdialysis systolic BP was significantly higher (159.0 versus 128.1 mmHg). Endothelial cell function was impaired among subjects with intradialytic hypertension as measured by decreased median ALDH(br) cells and decreased CD34(+)CD133(+) cells (ALDH(br), 0.034% versus 0.053%; CD34(+)CD133(+), 0.033% versus 0.059%). FMD was lower among subjects with intradialytic hypertension (1.03% versus 1.67%).
  
  
  CONCLUSIONS
  Intradialytic hypertension is associated with endothelial cell dysfunction. We propose that endothelial cell dysfunction may partially explain the higher event rates observed in these patients.
authors.affiliation: UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8523, USA. jula.inrig@utsouthwestern.edu
authors.forename: Jula K
authors.initials: JK
authors.lastname: Inrig
authors.forename: Peter
authors.initials: P
authors.lastname: Van Buren
authors.forename: Catherine
authors.initials: C
authors.lastname: Kim
authors.forename: Wanpen
authors.initials: W
authors.lastname: Vongpatanasin
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Povsic
authors.forename: Robert D
authors.initials: RD
authors.lastname: Toto
mesh_terms: D000071916:AC133 Antigen; D000328:Adult; D000368:Aged; D000446:Aldehyde-Lyases / Q000097:blood; D015703:Antigens, CD / Q000097:blood; D018952:Antigens, CD34 / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D018660:Blood Pressure Monitoring, Ambulatory; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D042783:Endothelial Cells / Q000378:metabolism; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D005434:Flow Cytometry; D006023:Glycoproteins / Q000097:blood; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D010455:Peptides / Q000097:blood; D011446:Prospective Studies; D006435:Renal Dialysis / Q000009:adverse effects*; D013234:Stem Cells / Q000378:metabolism; D013781:Texas; D018617:Ultrasonography, Doppler, Pulsed; D014664:Vasodilation
chemical_list: D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; D015415:Biomarkers; D006023:Glycoproteins; C000606023:PROM1 protein, human; D010455:Peptides; D000446:Aldehyde-Lyases; C043439:aldehyde decarbonylase