The factor V Leiden (R506Q) mutation and risk of thrombosis in renal transplant recipients

被引:65
作者
Irish, AB
Green, FR
Gray, DWR
Morris, PJ
机构
[1] UNIV OXFORD, JOHN RADCLIFFE HOSP, NUFFIELD DEPT SURG, OXFORD OX3 9DU, ENGLAND
[2] CHURCHILL HOSP, OXFORD TRANSPLANT CTR, OXFORD OX3 7LJ, ENGLAND
关键词
D O I
10.1097/00007890-199708270-00010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background. Renal transplantation and chronic renal failure are associated with an increased risk of venous thrombosis and myocardial infarction (MI). We investigated whether resistance to activated protein C due to a mutation in the factor V gene (FV Leiden/FV506Q) may predispose patients to thrombosis. Methods. Three hundred patients who had undergone renal transplantation were genotyped for the FV mutation. Seventy-seven patients who had suffered thrombotic complications (42 venous, 28 arterial, and 7 both) were compared with 223 patients free of thrombosis. Results. Thirty-two patients had suffered early renal allograft thrombosis (30 venous), and 33 patients had suffered MI, A higher proportion of the patients with thrombosis, compared to those without, had a family history of arterial cardiovascular disease (42% vs, 26%, P=0.04). Eighteen (6%) patients were heterozygous for FV506Q and seven (39%) of these had suffered venous thrombosis (including four primary allograft thromboses), compared with 15% of the patients without the mutation (P<0.05). The odds ratio for risk of venous thrombosis for FV506Q carriers was 3.6 (95% confidence interval: 1.3-9.9) or 4.0 (1.2-13.8) for primary allograft thrombosis. Only one of the FV506Q carriers had suffered an MI. Conclusions. Carriers of the factor V 506Q mutation with chronic renal failure who have undergone transplantation are at an increased risk of venous but not arterial thrombosis. This mutation explained 14% of all venous and 20% of primary allograft thrombosis, suggesting that other unidentified genetic and environmental factors contribute to the risk of thrombosis in renal transplant recipients.
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页码:604 / 607
页数:4
相关论文
共 22 条
[1]  
ALLEN RDM, 1987, SURG GYNECOL OBSTET, V164, P137
[2]   MUTATION IN BLOOD-COAGULATION FACTOR-V ASSOCIATED WITH RESISTANCE TO ACTIVATED PROTEIN-C [J].
BERTINA, RM ;
KOELEMAN, BPC ;
KOSTER, T ;
ROSENDAAL, FR ;
DIRVEN, RJ ;
DERONDE, H ;
VANDERVELDEN, PA ;
REITSMA, PH .
NATURE, 1994, 369 (6475) :64-67
[3]  
BERTINA RM, 1995, THROMB HAEMOSTASIS, V74, P449
[4]  
COHEN H, 1988, Fibrinolysis, V2, P197, DOI 10.1016/0268-9499(88)90013-6
[5]  
DAHLBACK B, 1995, THROMB HAEMOSTASIS, V74, P139
[6]  
DAWSON SJ, 1993, J BIOL CHEM, V268, P10739
[7]   DECREASE IN ENDOTHELIAL CELL-DEPENDENT PROTEIN-C ACTIVATION INDUCED BY THROMBOMODULIN BY TREATMENT WITH CYCLOSPORINE [J].
GARCIAMALDONADO, M ;
KAUFMAN, CE ;
COMP, PC .
TRANSPLANTATION, 1991, 51 (03) :701-705
[8]  
GRAY DWR, 1994, KIDNEY TRANSPLANTATI, P314
[9]  
GREEN F, 1993, THROMB HAEMOSTASIS, V70, P915
[10]  
IBELS LS, 1977, Q J MED, V46, P197