title: Associations of endothelial dysfunction and arterial stiffness with intradialytic hypotension and hypertension.
abstract: Intradialytic hypotension and hypertension are both independently associated with mortality among persons with end-stage renal disease on hemodialysis. Endothelial dysfunction and arterial stiffness are two possible mechanisms underlying these phenomena, but their association with hemodynamic instability during dialysis has not been evaluated. Thirty patients were recruited from chronic dialysis units at San Francisco General Hospital and San Francisco Veterans Affairs Medical Center. Endothelial dysfunction was assessed with flow-mediated dilation of the brachial artery after upper arm occlusion. Arterial stiffness was assessed using carotid-femoral pulse wave velocity measured by tonometry. Intradialytic hypotension and hypertension were defined as the average decrease in systolic blood pressure (SBP) over 1 week, as well as the frequency over 1 month of hypotension or hypertension. Every 5% decrease in flow-mediated dilation was associated with a 7.5 mmHg decrease in SBP after adjustment for phosphorus, body mass index, atherosclerosis, and ultrafiltration (P=0.02). Every 5 m/s increase in pulse wave velocity was associated with an 8 mmHg increase in SBP after adjustment for predialysis SBP and ultrafiltration (P=0.03). Over 1 month, every 5% lower flow-mediated dilation was associated with a 10% higher frequency of hypotension (P=0.09), and every 5 m/s increase in pulse wave velocity was associated with an 15% higher frequency of hypertension (P=0.02). In a cross-sectional analysis of 30 dialysis patients, endothelial dysfunction and arterial stiffness were independently associated with intradialytic hypotension and intradialytic hypertension, respectively. Elucidating these potential mechanisms of hemodynamic instability during dialysis may facilitate development of treatment strategies specific to this pathophysiology.
authors.affiliation: Department of Medicine, Division Nephrology, University of California, San Francisco, California 94143-0532, USA. ruth.dubin@ucsf.edu
authors.forename: Ruth
authors.initials: R
authors.lastname: Dubin
authors.forename: Christopher
authors.initials: C
authors.lastname: Owens
authors.forename: Warren
authors.initials: W
authors.lastname: Gasper
authors.forename: Peter
authors.initials: P
authors.lastname: Ganz
authors.forename: Kirsten
authors.initials: K
authors.lastname: Johansen
mesh_terms: D000368:Aged; D001794:Blood Pressure; D001916:Brachial Artery / Q000503:physiopathology*; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006339:Heart Rate; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000401:mortality / Q000503:physiopathology*; D007022:Hypotension / Q000209:etiology / Q000401:mortality / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis / Q000009:adverse effects*; D013997:Time Factors