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
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.