E. Yoshida et al., IMPAIRED HIGH-SHEAR-STRESS-INDUCED PLATELET-AGGREGATION IN PATIENTS WITH CHRONIC-RENAL-FAILURE UNDERGOING HEMODIALYSIS, British Journal of Haematology, 89(4), 1995, pp. 861-867
We investigated shear-induced platelet aggregation (SIPA) in 30 patien
ts with chronic renal failure (CRF) undergoing haemodialysis. 26 patie
nts showed a significant decrease in SIPA at high shear stress but no
change in SIPA at low shear stress. The former reaction reflects the i
nteraction between plasma non Willebrand factor (vWF) and its platelet
receptors, glycoprotein (GP) Ib-M and IIb/IIIa complex, whereas the l
atter 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 ra
tio of ristocetin cofactor/vWF antigen in plasma was slightly lower in
CRF patients than in controls (P<0.01). However, the level of GPIb an
tigen in the platelets of these patients was significantly reduced (42
.1+/-20.3% of normal platelets), with partial destruction of GPIb anti
gen, The number of VWF receptors on the GPIb molecule was quantitated
using the GPIb-binding protein alboaggregin-B (AL-B), purified from th
e snake venom of Trimeresurus albolabris. AL-B bound to GPIb at a tota
l 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 9
80+/-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 CR
F patients is due to both abnormalities in plasma vWF and in its plate
let GPIb receptor.