HEMODYNAMIC-CHANGES INDUCED BY THE CORRECTION OF ANEMIA BY ERYTHROPOIETIN - ROLE OF ANTIPLATELET THERAPY

Citation
F. Caravaca et al., HEMODYNAMIC-CHANGES INDUCED BY THE CORRECTION OF ANEMIA BY ERYTHROPOIETIN - ROLE OF ANTIPLATELET THERAPY, Nephrology, dialysis, transplantation, 10(9), 1995, pp. 1720-1724
Citations number
24
Categorie Soggetti
Urology & Nephrology",Transplantation
ISSN journal
09310509
Volume
10
Issue
9
Year of publication
1995
Pages
1720 - 1724
Database
ISI
SICI code
0931-0509(1995)10:9<1720:HIBTCO>2.0.ZU;2-V
Abstract
Background. In a restrospective study, antiplatelet therapy has been s hown to be associated with a decreased incidence of erythropoietin-ind uced hypertension. In order to ascertain the role of antiplatelet drug s in the haemodynamic response to the correction of anaemia by rHuEpo, 18 patients on chronic haemodialysis who started rHuEpo therapy were prospectively studied. Methods. The subjects were randomly assigned to receive or not, one of the following antiplatelet drugs: ditazole (3 patients), ticlopidine (3 patients) or aspirin plus dipyridamole (3 pa tients). Cardiac index (CI) by echo-Doppler, total peripheral resistan ce (TPR) and mean arterial pressure (MAP) were determined at baseline 10 and 20 weeks following the initiation of rHuEpo therapy. rHuEpo the rapy was administered subcutaneously at the same dose (40 U/kg thrice weekly) during the first 10 weeks. Ten uraemic patients on haemodialys is who had never received rHuEpo therapy served as the control group. Results. One patient in the group without antiplatelet drugs discontin ued the study due to the development of severe hypertension after 12 w eeks on rHuEpo therapy. There were no significant differences in the h aemodynamic parameters at baseline. At 10 weeks, MAP was higher in pat ients without than with antiplatelet drugs or controls untreated with rHuEpo (128.5 +/- 28 versus 100.6 +/- 13.5 versus 98.7 +/- 14 mmHg res pectively, P = 0.0047), TPR was also higher in patients without antipl atelet drugs than in the 2 other groups (1919 +/- 433 versus 1576 +/- 359 versus 1418 +/- 324 din.seg.cm(-5)m(2) respectively, P = 0.0231), but CI did not differ among the three groups. At 20 weeks, MAP was sti ll higher in patients without antiplatelet drugs than in patients with antiplatelet drugs or controls not on rHuEpo therapy respectively (11 2.9 +/- 24.6 versus 91.0 +/- 9.0 versus 101.7 +/- 14.1 mmHg respective ly, P = 0.075), but at this stage TPR and Cl did not differ among the three groups. Conclusions. These data reinforce the previous observati on that antiplatelet therapy may prevent the development of rHuEpo-ind uced hypertension.