Plasma and platelet von Willebrand factor abnormalities in patients with uremia: Lack of correlation with uremic bleeding

Citation
A. Casonato et al., Plasma and platelet von Willebrand factor abnormalities in patients with uremia: Lack of correlation with uremic bleeding, CL APPL T-H, 7(2), 2001, pp. 81-86
Citations number
28
Categorie Soggetti
Hematology
Journal title
CLINICAL AND APPLIED THROMBOSIS-HEMOSTASIS
ISSN journal
10760296 → ACNP
Volume
7
Issue
2
Year of publication
2001
Pages
81 - 86
Database
ISI
SICI code
1076-0296(200104)7:2<81:PAPVWF>2.0.ZU;2-E
Abstract
Chronic renal failure often is associated with abnormal bleeding that may r epresent an important complication of this disorder. The hemorrhagic tenden cy currently is attributed to altered primary hemostasis, mainly platelet d ysfunction. However, von Willebrand factor (VWF) also seems to be involved, even though the nature of its abnormalities is still controversial. To gai n insight into the role of VWF in determining uremic bleeding, we studied 1 1 patients with stable, chronic renal failure. We found a significant incre ase in plasma factor VIII (FVIII), vWF:antigen (Ag), and vWF:ristocetin cof actor (Rco) levels, associated with a mean decrease in platelet vWF:Ag. Pla sma VWF multimer pattern was characterized by increased representation of a ll oligomers in all patients, but five patients also showed a slight decrea se in large vWF multimers. In addition, platelet vWF multimer pattern displ ayed a decrease in all components, especially those with high molecular wei ght. Despite normal bleeding time, collagen-induced platelet aggregation wa s defective in almost all patients, whereas vWF collagen binding capacity w as normal. The levels of glycocalicin, the circulating fragment of glycopro tein Ib-IX, the major plate let vWF receptor, were also normal. In six pati ents who also were studied after initiation of dialysis, collagen-induced p late let aggregation was impaired further. Moreover, plasma vWF, and especi ally FVIII levels, were increased additionally, in association with a norma lized platelet VWF content and an improved vWF multimer pattern. The result s suggest that vWF abnormalities are present in uremia. Moreover, thrombopa thy caused by impaired collagen-induced platelet aggregation is constantly present and apparently not improved by dialytic treatment.