Nephrology Dialysis Transplantation, Vol 13, Issue 3 679-684, Copyright © 1998 by Oxford University Press
A Irish and F Green
Background: Factor VII coagulant activity (VIIc) is
implicated in cardiovascular disease (CVD) risk in the general population.
VIIc is correlated with hyperlipidaemia and influenced by a polymorphism of
the factor VII gene and could contribute to thrombotic risk in patients
with renal disease. Methods: We studied VIIc in 100
patients with chronic renal disease or on maintenance dialysis and examined
its relationship with dyslipidaemia, a marker of coagulation activation
prothrombin fragment F1+2 (F1+2), the acute-phase reactant and coagulation
factor fibrinogen, a mediator of the inflammatory response interleukin-6
(IL6), and the factor VII R353Q polymorphism.
Results:VIIc (186±58
vs 140±37, % standard, P<0.0001) and
F1+2 (0.51 vs 0.30 nM, median, P<0.0001) were
increased in the patients with renal disease compared with the control
group, consistent with a hypercoagulable state. Patients and controls
heterozygous for the factor VII R353Q polymorphism, had 35% lower VIIc than
homozygotes for the R353 allele, indicating that the Q353 allele could
confer genetic protection from thrombotic risk. There was a significant
correlation between VIIc and F1+2 (r=0.26, P<0.05), total and VLDL
cholesterol, and triglycerides, but the correlation with lipids did not
differ by genotype. VIIc and F1+2 also correlated with increased
concentration of IL6 and fibrinogen, and inversely with albumin, suggesting
that a persistent inflammatory response could contribute to a
hypercoagulable state, possibly via cytokine induced activation of the
endothelium, or by induction of monocytes to express tissue factor.
Patients with CVD complications or a history of myocardial infarction did
not have higher VIIc or F1+2 than those without CVD.
Conclusions: VIIc was significantly increased in renal
disease states and strongly influenced by a common polymorphism of the
factor VII gene, but the increase in VIIc and its correlation with lipids
was not genotype specific. VIIc correlated with evidence of increased
coagulation activation and persistence of an inflammatory response. A
persistent inflammatory response and the dyslipidaemia of renal disease may
contribute to coagulation activation and increased cardiovascular risk.
Prospective studies are required to evaluate increased VIIc as a thrombotic
risk factor in chronic renal disease. Key words:
chronic renal disease; dyslipidaemia; factor II genotype; factor VII
coagulant activity (VIIc); interleukin 6; prothrombin fragment F1+2
ORIGINAL ARTICLES
Factor VII coagulant activity (VIIc) and hypercoagulability in chronic renal disease and dialysis: relationship with dyslipidaemia, inflammation, and factor VII genotype
The Renal Unit, The Churchill Hospital, UK; Corresponding author at: Nuffield Department of Surgery, John Radcliffe Hospital, Headington, Oxford, UK
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J. A. D'Elia, L. A. Weinrauch, R. E. Gleason, I. Lipinska, J. Keough, S. Pendse, B. Roshan, A. T. Lee, and G. H. Tofler Fibrinogen and Factor VII Levels Improve With Glycemic Control in Patients With Type 1 Diabetes Mellitus Who Have Microvascular Complications Arch Intern Med, January 8, 2001; 161(1): 98 - 101. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Irish Renal allograft thrombosis: can thrombophilia explain the inexplicable? Nephrol. Dial. Transplant., October 1, 1999; 14(10): 2297 - 2303. [Full Text] [PDF]
|
|