title: Platelet surface receptor activation in patients with chronic renal failure on hemodialysis, peritoneal dialysis and those with successful kidney transplantation.
abstract: Hemostatic disorders associated with chronic renal failure (CRF) include hemorrhagic and/or thrombotic manifestations, which were ascribed, in part, to uremic platelet dysfunction including abnormalities of expression of platelet glycoprotein receptors. There is, however, still no general agreement on the exact characterization of these platelet abnormalities. This study aims at characterizing the platelet glycoprotein abnormalities associated with CRF, by recording the effect of the three renal replacement therapies, hemodialysis (HD), chronic ambulatory peritoneal dialysis (CAPD), and renal transplantation, on these receptors. The study, which was mainly cross-sectional, included two groups: (i) Patient groups (n = 50): HD patients (n = 20), CAPD patients (n = 10) and successful renal transplant patients (n = 20); (ii) Healthy Controls (n = 34): 23 were men and 11 were women who were age- and sex-matched with the patients. Flow cytometric quantitation of CD41, CD42a, CD42b and CD61 was carried out using a Becton-Dickinson FACScan. The expression of CD41 levels showed a highly significant increase in HD and CAPD patients when compared with the normal control levels. However, levels in transplant patients were comparable to the normal control levels. On the other hand, the expression of CD42a, CD42b, and CD61 showed no significant change in HD and CAPD patients when compared with normal control levels, but there was a significant decrease in transplant patients when compared to the normal control levels. In conclusion, there was evidence of increased expression of one glycoprotein receptor (GpIIb-IIIa) pre-dialysis whether HD or CAPD. In transplant patients, no evidence of platelet activation could be demonstrated.
authors.affiliation: King Fahad, National Guard Hospital, Riyadh, Saudi Arabia.
authors.forename: A
authors.initials: A
authors.lastname: Ballow
authors.forename: A M A
authors.initials: AM
authors.lastname: Gader
authors.forename: S
authors.initials: S
authors.lastname: Huraib
authors.forename: K
authors.initials: K
authors.lastname: Al-Husaini
authors.forename: A
authors.initials: A
authors.lastname: Mutwalli
authors.forename: J
authors.initials: J
authors.lastname: Al-Wakeel
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D001792:Blood Platelets / Q000737:chemistry* / Q000473:pathology; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D016130:Immunophenotyping; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000628:therapy*; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D010530:Peritoneal Dialysis; D015539:Platelet Activation; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000032:analysis; D010980:Platelet Membrane Glycoproteins / Q000032:analysis*; D011956:Receptors, Cell Surface / Q000032:analysis*; D006435:Renal Dialysis
chemical_list: D015703:Antigens, CD; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D010980:Platelet Membrane Glycoproteins; D011956:Receptors, Cell Surface