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Impaired high‐shear‐stress‐induced platelet aggregation in patients with chronic renal failure undergoing haemodialysis
Author(s) -
Yoshida Eri,
Fujimura Yoshihiro,
Ikeda Yasuo,
Takeda Ichiroh,
Yamamoto Yasuhiro,
Nishikawa Kiyoshi,
Miyataka Kazuhiko,
Oonuki Masahiro,
Kawasaki Tomihisa,
Katayama Masahiko,
Narita Nobuhiro
Publication year - 1995
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1995.tb08425.x
Subject(s) - medicine , chronic renal failure , platelet , cardiology , hemodialysis , platelet aggregation , urology
We investigated shear‐induced platelet aggregation (SIPA) in 30 patients with chronic renal failure (CRF) undergoing haemodialysis. 26 patients showed a significant decrease in SIPA at high shear stress but no change in SIPA at low shear stress. The former reaction reflects the interaction between plasma von Willebrand factor (vWF) and its platelet receptors, glycoprotein (GP) Ib‐IX and lIb/ IlIa complex, whereas the latter is assumed to involve the binding of plasma fibrinogen to GP IIb/IIIa complex. These SIPA profiles in CRF patients after haemodialysis showed almost no change compared to those before haemodialysis. The ratio of ristocetin cofactor/vWF antigen in plasma was slightly lower in CRF patients than in controls (P<0.01). However, the level of GPIb antigen in the platelets of these patients was significantly reduced (42.1±20‐3% of normal platelets), with partial destruction of GPIb antigen. The number of vWF receptors on the GPIb molecule was quantitated using the GPIb‐binding protein alboaggregin‐B (AL‐B), purified from the snake venom of Trimeresurus albolabris. AL‐B bound to GPIb at a total of 48 760±9944 molecules per normal platelet and a K d of 85.44±15.70 nM at saturation. In contrast, binding in CRF platelets was 22 980±6395 molecules per platelet and K d was 50.08±13.83 nM. Taking these results together, we conclude that the impaired SIPA found in CRF patients is due to both abnormalities in plasma vWF and in its platelet GPIb receptor.