Thrombophilia and Thrombotic Problems in Renal Transplant Patients

Kujovich, Jody L.

doi:10.1097/01.tp.0000107185.50838.ee

Cited by 38 publications

(26 citation statements)

References 51 publications

(60 reference statements)

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“…Maior atenção tem sido voltada, nos últimos anos, à prevenção e ao controle dos eventos de natureza não imunológica, uma vez que o controle da resposta imune atualmente é efetivo e acompanhado de baixa incidência de disfunção aguda do enxerto atribuída a eventos imunológicos. A trombofilia é um importante fator de risco não imunoló-gico para a evolução do enxerto durante o primeiro ano após o transplante renal 1 . Caracteriza-se por uma tendência aumentada para a formação de trombos e pode ser classificada em primária (genética) ou secundária (adquiria).…”

Section: Introductionunclassified

Mutação G20210A no gene da protrombina, fator V de Leiden e anticorpos anticardiolipina não influenciam a sobrevida do enxerto renal após o transplante

Rocha¹,

Galante²,

Alvarez³

et al. 2009

J. Bras. Nefrol.

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Section: Introductionunclassified

Mutação G20210A no gene da protrombina, fator V de Leiden e anticorpos anticardiolipina não influenciam a sobrevida do enxerto renal após o transplante

Rocha¹,

Galante²,

Alvarez³

et al. 2009

J. Bras. Nefrol.

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“…Thromboembolic complications after renal transplant include an 8% risk of DVT or PE within the first month post transplant, with peak risk at 4 months post transplant. 42 Combined kidney pancreas transplants are associated with a 4-fold higher risk of proximal DVT or PE than kidney transplants alone. In addition, primary graft vessel thrombosis occurs in 1-7% of renal transplants and generally results in loss of graft function.…”

Section: Organ Transplantationmentioning

confidence: 99%

“…Perioperative anticoagulation is recommended for patients with thrombophilia and previous thrombosis with consideration of continued oral anticoagulation for up to 1 year. 42,51 Orthotopic liver transplantation (OLT) is more frequently associated with significant operative blood loss due to reduced levels of procoagulant factors, chronic DIC and enhanced fibrinolysis, depending on the stage of the transplant surgery. Several studies recently have attempted to address the contribution of FVL to post-OLT thrombosis.…”

Section: Organ Transplantationmentioning

confidence: 99%

Management of Hereditary Hypercoagulable Disorders

Bockenstedt¹

2006

Hematology

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The clinical management of individuals with hereditary hypercoaguable disorders has evolved from initial broad recommendations of lifelong anticoagulation after first event of venous thromboembolism to a more intricate individualized risk-benefit analysis as studies have begun to delineate the complexity of interactions of acquired and hereditary factors which determine the predilection to thrombosis. The contribution of thrombophilic disorders to risk of thrombotic complications of pregnancy, organ transplantation, central venous catheter and dialysis access placement have been increasingly recognized. The risk of thrombosis must be weighed against risk of long-term anticoagulation in patients with venous thromboembolism. Thrombophilia screening in select populations may enhance outcome. Initial DecisionsThe clinical management of individuals with hereditary hypercoagulable disorders has evolved from initial broad recommendations of lifelong anticoagulation after first event of venous thromboembolism (VTE) to a more intricate, individualized risk-benefit analysis as the complexity of interactions of acquired and hereditary factors that determine the predilection to thrombosis are now recognized. Important behind stratifying risk of recurrent events is the necessity of correctly identifying hereditary thrombophilic disorders, especially in circumstances in which laboratory results, e.g., mildly low antithrombin III (ATIII) or protein S levels, may be more indicative of a temporary acquired deficiency. The relevance of thrombophilic testing is debated, but most clinicians agree that prothrombotic assessment should be considered in individuals with unprovoked thrombosis at age less than 40 years, individuals who have had thrombosis at an unusual anatomic site or who have had repeated thromboses, or when the family history suggests multiple affected individuals. For review of the laboratory assessment of thrombophilia see references [1][2][3] . The following discussion is not meant to be comprehensive, but serves to highlight a few of the clinical management decisions important in the care of the thrombophilic patient. Therapeutic considerations involving individuals with antiphospholipid syndrome (APS) will be included where pertinent. Duration of anticoagulant therapyThe decision to extend therapy beyond 6-12 months after an incident thrombotic event must be made on an individual basis. Patients with a transient risk factor such as oral contraceptive use, postsurgical state or limb immobilization have a low risk of recurrence of thrombosis once anticoagulation has been completed. (For review see 4,5 .) Identifying the individual with moderate to high risk of recurrent thrombosis is important to prevent the unnecessary risk of hemorrhage from long-term anticoagulation. From studies of patients with a first VTE (both with and without diagnosed hereditary thrombophilia), one third of patients with unprovoked VTE will have a reoccurrence over the next 10 years and 6% of patients with VTE develop postphlebitic syndrom...

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“…9 In addition, homozygosity in T677 mutation in the MTHFR gene that causes hyper- homocysteinemia, is thought to be an independent risk factor for venous thromboembolism. 8 Coexistence of both mutations regarding FVL and MTHFR and their involvement to renal allograft thrombosis, remains unknown. We present a successful living-related renal transplant in a recipient with inherited thrombophilia because of heterozygosity for mutation of factor V Q506 and homozygosity for mutation T677 for MTHFR.…”

Section: Introductionmentioning

confidence: 99%

“…8 Placement of arginine instead of glutamine at residue 506 leads to a defective molecule of factor V that hinders combination to activated protein C and thus inhibits normal creation of thrombi. It presents with idiopathic deep venous thrombosis in heterozygotic carriers.…”

Section: Introductionmentioning

confidence: 99%

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Florou

Koukoulaki²,

Theodoros³

et al. 2017

Exp Clin Transplant

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Thrombophilia due to activated protein C resistance (Leiden mutation) is the most common inherited thrombophilic disorder with 5% incidence in whites. Renal transplant of these patients entails a risk of vascular thrombosis soon after the transplant; and acute rejection episodes and graft loss within the first year. We present a case of a successful living-related renal transplant in man with a recent history of repeat episodes of vascular access thrombosis attributed to inherited thrombophilia (heterozygosity for factor V mutation Q506 and homozygosity for mutation T677 for methylenetetrahydrofolate reductase). Transplant recipient was administered anticoagulation therapy with low molecular weight heparin pre-and postoperatively. No thrombotic or hemorrhagic events occurred posttransplant. A high suspicion of thrombophilic disorders in patients with end-stage renal disease with vascular access thrombotic events should be screened further to prevent failure of a subsequent renal transplant. Inherited thrombophilic disorders may not exclude living-related kidney transplant provided that anticoagulation therapy is administered perioperatively.

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Thrombophilia and Thrombotic Problems in Renal Transplant Patients

Cited by 38 publications

References 51 publications

Mutação G20210A no gene da protrombina, fator V de Leiden e anticorpos anticardiolipina não influenciam a sobrevida do enxerto renal após o transplante

Mutação G20210A no gene da protrombina, fator V de Leiden e anticorpos anticardiolipina não influenciam a sobrevida do enxerto renal após o transplante

Management of Hereditary Hypercoagulable Disorders

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