Thromb Haemost 1968; 20(01/02): 267-284
DOI: 10.1055/s-0038-1651266
Originalarbeiten – Original Articles – Travaux Originaux
Schattauer GmbH

Formation, Consistency and Degradation of Artificial Thrombi in Severe Renal Failure

Effect of A B 0 Blood Groups
L Dintenfass*
1   Department of Medicine, University of Sydney, and the Haemorheology Unit and Kanematsu Institute, Sydney Hospital, Sydney, Australia
,
J. H Stewart**
1   Department of Medicine, University of Sydney, and the Haemorheology Unit and Kanematsu Institute, Sydney Hospital, Sydney, Australia
› Author Affiliations
Further Information

Publication History

Publication Date:
27 June 2018 (online)

Summary

A novel study of dynamic blood coagulation in uraemic patients was based on the application of the variable-frequency thromboviscometer, VFTV, an advanced form of the thrombelastograph. Clotting times, rates of formation, consistencies, and rates of degradation of artificial thrombi cast at 60 and 180 cycles/min (equal to mean shear rates of 26.8 and 80 sec–1) were investigated in 35 patients and in normal controls.

The study shows that there exists a profound difference in VFTV parameters between normals and patients with severe renal failure. The most significant are the rate of degradation of thrombi formed at 60 cycles/min (p < 0.001), the consistency of thrombi formed at 180 cycles/min (p < 0.005), and the total thrombus formation time at 180 cycles/min (p < 0.001). Thrombi formed at 60 cycles/min adhered to brass rather than Teflon in many patients with renal failure, in contrast to the findings in normals and in all types of patients previously tested.

A division of patients into clinical subgroups (acute renal failure, non-oliguric or oliguric chronic renal failure, and long-term dialysis) shows that all these groups are quite homogeneous from the dynamic coagulation viewpoint, although the thrombus degradation rate (when coagulation proceeds at 60 cycles/min) differs significantly (p = 0.025) between the long-term dialysis group and the non-oliguric chronic renal failure group. These same groups also show a difference in their platelet count. The VFTV abnormalities of uraemia could not be correlated with either the severity of the measurable biochemical derangement or the qualitative platelet defect.

An unexpected, but statistically significant, pattern appeared when patients were divided according to their ABO blood groups. The rate of degradation of the thrombus formed at 60 cycles/min differed significantly between 0 and A and between B and A blood groups (p < 0.01). The rate of formation of the white thrombus at 180 cycles/ min differed significantly (p < 0.05) between 0 and A blood groups. Simultaneously, the platelet count differed between blood groups 0 and B (p = 0.05) and between 0 and A (p < 0.005).

Effect of blood groups on the VFTV parameters is evident even in the normal controls; here, the rate of degradation of the thrombus formed at 60 cycles/min showed significant difference between blood groups A and B (p < 0.005) and a smaller difference between 0 and B(0.05 < p <0.1).

We consider that the demonstration that the consistency of white thrombi is twice as high in uraemic patients than in normals, and that the rate of degradation of the red-white thrombi is nearly ten-fold greater is of fundamental importance. Both these phenomena might be associated with the known platelet defects of uraemia, or with a possible further abnormalities of fibrinogen, caused by the presence of one or more of the chemical substances which accumulate in the uraemic state.

* Senior Research Fellow of the National Heart foundation of Australia at the Department of Medicine, University of Sydney, and Honorary Consulting Biorheologist, Haemorheology Unit, Sydney Hospital.


** Renal Physician, Medical Research Department, Sydney Hospital.


 
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