title: Biphasic effects of hemodialysis on platelet reactivity in patients with end-stage renal disease: a potential contributor to cardiovascular risk.
abstract: BACKGROUND
  Cardiovascular disease is rampant in patients with end-stage renal disease (ESRD), and increased platelet reactivity may contribute. This study is designed to determine effects of hemodialysis in patients with ESRD on platelet reactivity per se.
  
  
  METHODS
  Platelet reactivity was determined by flow cytometry in 36 patients with ESRD undergoing hemodialysis. Blood was obtained from arterial and venous ends of the hemodialysis circuit at the beginning and end of the dialysis session. Platelet reactivity was defined with respect to capacity to bind fibrinogen (activation of glycoprotein IIb-IIIa) and expression of P-selectin in response to adenosine diphosphate (ADP; 0, 0.2, and 1.0 micromol/L). Comparison studies were performed with 55 patients with coronary artery disease (CAD) and 38 healthy subjects.
  
  
  RESULTS
  Platelet reactivity was increased by exposure to the dialysis circuit (capacity to bind fibrinogen: arterial, 28% +/- 13%; venous, 47% +/- 20%; P < 0.001). Despite this effect, surface expression of P-selectin in response to 1 micromol/L of ADP was lower at the end of the dialysis session (arterial blood at its onset, 40% +/- 16%; arterial blood at its conclusion, 24% +/- 15%; P < 0.05). Confocal microscopy showed increased nonspecific association of fibrinogen with platelets after dialysis, suggesting that increased aggregation after dialysis may be secondary to effects of dialysis on fibrinogen binding, rather than on platelet reactivity. Platelet reactivity was increased similarly in patients with ESRD and those with CAD compared with healthy subjects.
  
  
  CONCLUSIONS
  Although interaction between platelets and the dialysis circuit increases platelet reactivity, continued dialysis decreases platelet reactivity.
authors.affiliation: Department of Medicine, The University of Vermont College of Medicine, Burlington, VT 05401, USA. atul.aggarwal@vtmednet.org
authors.forename: Atul
authors.initials: A
authors.lastname: Aggarwal
authors.forename: Samer S
authors.initials: SS
authors.lastname: Kabbani
authors.forename: Jeffery M
authors.initials: JM
authors.lastname: Rimmer
authors.forename: F John
authors.initials: FJ
authors.lastname: Gennari
authors.forename: Douglas J
authors.initials: DJ
authors.lastname: Taatjes
authors.forename: Burton E
authors.initials: BE
authors.lastname: Sobel
authors.forename: David J
authors.initials: DJ
authors.lastname: Schneider
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D003324:Coronary Artery Disease / Q000097:blood; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000628:therapy*; D008297:Male; D008567:Membranes, Artificial; D018613:Microscopy, Confocal; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology; D019007:P-Selectin / Q000378:metabolism; D015539:Platelet Activation / Q000187:drug effects / Q000502:physiology; D010974:Platelet Aggregation / Q000187:drug effects / Q000502:physiology; D010979:Platelet Function Tests / Q000379:methods; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000378:metabolism; D011485:Protein Binding / Q000187:drug effects / Q000502:physiology; D006435:Renal Dialysis / Q000009:adverse effects / Q000379:methods*; D012307:Risk Factors
chemical_list: D008567:Membranes, Artificial; D019007:P-Selectin; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000244:Adenosine Diphosphate; D005340:Fibrinogen