Journal Article

Inverse relationships between haemoglobin and ristocetin-induced platelet aggregation in haemodialysis patients under erythropoietin therapy

J. Borawski, A. Rydzewski, M. Mazerska, M. Kalinowski, K. Pawalak and M. Mysliwiec

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 11, issue 12, pages 2444-2448
Published in print December 1996 | ISSN: 0931-0509
e-ISSN: 1460-2385 | DOI: http://dx.doi.org/10.1093/oxfordjournals.ndt.a027212
Inverse relationships between haemoglobin and ristocetin-induced platelet aggregation in haemodialysis patients under erythropoietin therapy

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Background.

Amelioration of the anaemia of chronic renal failure and subsequent improved haemorheology result in correction of bleeding diathesis as evidenced by shortening of the skin bleeding time (BT). However, the relationship between the haematocrit and platelet-vessel wall interactions in haemodialysis (HD) patients under recombinant human erythropoietin (rHuEpo) therapy, assessed by platelet aggregation in response to ristocetin is more complex and somewhat inconsistent.

Methods.

We investigated the relationship between haemoglobin (Hb) levels and whole blood ristocetininduced platelet aggregation (electric impedance method) in 28 HD patients treated with rHuEpo, and with normal BT. The measurements were repeated in 16 subjects after having reduced platelet aggregability with orally administered ketanserin.

Results.

Ristocetin-induced platelet aggregation in the whole group was comparable to those found in 21 age-matched healthy subjects (normals) and in 25 HD patients not treated with rHuEpo (uraemics). Interestingly, a significant inverse correlation between this aggregation and Hb concentration was found (r = −0.392, P<0.05). In the group of 16 patients, the preketanserin aggregation was more intensive than in the normals and uraemics (P<0.05). Ketanserin produced a fall in ristocetin-induced platelet aggregation (P<0.02), prolongation of the BT (P<0.02) and, unexpectedly, a decrease in serum Epo concentration (P<0.0002) and the Hb level (P<0.001). Again, an inverse correlation between depressed ristocetin-induced platelet aggregation and lowered Hb concentration was found (r= −0.590, P<0.02). Moreover, a strong positive correlation between the extent of preketanserin platelet aggregation and the decrease in the intensity of this process that followed the trial was observed (r=0.919, P<0.000005). There were no changes in other haematological parameters or arterial blood pressure.

Conclusions.

Considering the role of von Willebrand factor and fibrinogen in mediating ristocetin-induced platelet aggregation, and enhanced synthesis and/or release of these macromolecules in response to uraemia or inflammation, we suggest that exaggerated whole-blood platelet aggregability to ristocetin points to blunted erythropoiesis in HD patients on rHuEpo therapy.

Keywords: erythropoietin; ketanserin; platelet aggregation; ristocetin; uraemia

Journal Article.  0 words. 

Subjects: Nephrology

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