מתוך medicontext.co.il
WESTPORT, CT (Reuters Health) – The G20210A mutation in the prothrombin gene increases the risk of renal graft failure, according to a report in the November issue of the American Journal of Kidney Diseases.
The G20210A mutation in the prothrombin gene leads to significantly increased levels of circulating prothrombin and, consequently, a state of hypercoagulability, the authors explain. How this might affect renal transplantation outcomes had not been clear.
Dr. Michael Fischereder from Klinikum der Universitהt Regensburg in Germany compared renal graft survival in 270 consecutive renal transplant recipients, nine (3.7%) of whom proved to be heterozygous for the G20210A nucleotide substitution.
Patients with G20210A had median transplant survival less than half that of wild-type patients (65.9 months versus 149 months, p = 0.02), the authors report.
Among the five transplant failures in the G20210A group, three resulted from thrombotic events, the report indicates.
The heterozygous G20210A state was independently associated with a 2.95-fold increased risk for reduced transplant survival, the researchers note. Among first-time transplant recipients, the risk was increased even more, to 3.48-fold.
Other recognized risk factors did not differ between the two groups, the results indicate.
"Therefore," the authors conclude, "the G20210A mutation of the prothrombin gene should be considered an important risk factor for graft loss."
"Thrombophilia is a risk factor for allograft failure," Dr. Fischereder told Reuters Health. Thromboembolic complications should be thoroughly investigated when a patient history is taken, he added.
"Considering these data and the impact of thrombophilia on morbidity and graft survival in transplant recipients," the investigators write, "we believe prospective trials on the effect of therapeutic anticoagulation after renal transplantation are warranted."
"I would not favor unconditional therapeutic anticoagulation in the presence of thrombophilia without previous events," Dr. Fischereder said, "but…some colleagues have adopted this practice."
"The identification of genetic determinants for the susceptibility to disease offers us the opportunity not only to tailor therapy to the individual need, but also to define mechanisms of pathogenesis and identify new therapeutic options," Dr. Barbara Murphy, from Mount Sinai School of Medicine in New York, comments in a related commentary.
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