Is AV Fistula Patency Associated with Angiotensin-Converting Enzyme (ACE) Polymorphism and ACE Inhibitor Intake?

Heine, Gunnar H.; Ulrich, Christof; Köhler, Hans; Girndt, Matthias

doi:10.1159/000080464

Cited by 29 publications

(35 citation statements)

References 35 publications

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“…In this study, renin-angiotensin system inhibition was observed as having limited ability to prevent AV stenosis. 32 The limitations of this study were insufficient II allele and lack of information in some patients about the usage of ACEI and AT-1 antagonist. We also noticed that usage of ACEI and ARB did not prevent early-stage AVF thrombosis.…”

Section: Discussionmentioning

confidence: 89%

The Presence of PAI-1 4G/5G and ACE DD Genotypes Increases the Risk of Early-Stage AVF Thrombosis in Hemodialysis Patients

et al. 2011

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Background: In this study, we investigated the relationship between early arteriovenous fistula (AVF) thrombosis with angiotensin-converting enzyme (ACE) gene and thrombophilic factor gene polymorphisms. Methods: Thirty-five patients who suffered from three or more fistula thrombosis episodes in the early period after AVF operation and 33 control patients with no history of thrombosis for at least 3 years were enrolled in this study. Results: Factor V G1691A Leiden, factor V H1299R (R2), prothrombin G20210A, factor XIIIV34L, b-fibrinogen-455 G-A, glycoprotein IIIa L33P human platelet antigens (HPA-1), methylenetetrahydrofolate reductase C677T, and methylenetetrahydrofolate reductase A1298C gene polymorphisms were similar in both groups (p > 0.05). Plasminogen activator inhibitor 1 (PAI-1) 4G/5G genotype in the study group and 4G/4G genotype in the control group were significantly higher (p = 0.014). No significant difference was detected in terms of the 5G/5G genotype. With regard to the ACE gene polymorphism, the control group showed more ID genotype (19/33, 57.6%), whereas the study group showed more DD genotype (17/35, 48.6%). II genotype was similar in both groups (x 2 = 7.40, p = 0.025). The rate of ACE inhibitor-angiotensin II receptor blockers use was 5/35 in the study group (14.3%) and 5/33 in the control group (15.2%). Individuals with PAI-1 4G/5G genotype showed 5.03 times more risk of thrombosis when compared with 4G/4G and 5G/5G genotypes [p = 0.008, OR = 5.03, 95% confidence interval (1.44:17.64)]. Individuals with ACE DD genotype showed 4.25 times more risk of thrombosis when compared with II and ID [p = 0.008, OR = 4.25, 95% confidence interval (1.404:12.83)]. Conclusion: PAI-1 4G/5G and ACE DD genotypes are associated with increased risk for early AVF thrombosis.

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Section: Discussionmentioning

confidence: 89%

The Presence of PAI-1 4G/5G and ACE DD Genotypes Increases the Risk of Early-Stage AVF Thrombosis in Hemodialysis Patients

et al. 2011

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“…This interindividual variation may relate to differences in the genetic background that may influence susceptibility to vascular inflammation and neointima formation after endothelial and smooth muscle injury. 6,7 Consistent with this notion, AVF survival was reported to be associated with specific genetic polymorphisms of transforming growth factor (TGF)-␤1 8 and methylene tetrahydrofolate reductase. 9 In addition, we recently identified a length polymorphism in the heme oxygenase-1 (HO-1) gene that is associated with patency of AVFs.…”

mentioning

confidence: 78%

Far Infrared Therapy Inhibits Vascular Endothelial Inflammation via the Induction of Heme Oxygenase-1

Lin¹,

Liu

Peyton

et al. 2008

ATVB

117

115

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Objective-Survival of arteriovenous fistulas (AVFs) in hemodialysis patients is associated with both far infrared (FIR) therapy and length polymorphisms of the heme oxygenase-1 (HO-1) promoter. In this study, we evaluated whether there is an interaction between FIR radiation and HO-1 in regulating vascular inflammation. Methods and Results-Treatment of cultured human umbilical vein endothelial cells (ECs) with FIR radiation stimulated HO-1 protein, mRNA, and promoter activity. HO-1 induction was dependent on the activation of the antioxidant responsive element/NF-E2-related factor-2 complex, and was likely a consequence of heat stress. FIR radiation also inhibited tumor necrosis factor (TNF)-␣-mediated expression of E-selectin, vascular cell adhesion molecule-1, intercellular cell adhesion molecule-1, monocyte chemoattractant protein-1, interleukin-8, and the cytokine-mediated adhesion of monocytes to ECs. The antiinflammatory action of FIR was mimicked by bilirubin, and was reversed by the HO inhibitor, tin protoporphyrin-IX, or by the selective knockdown of HO-1. Finally, the antiinflammatory effect of FIR was also observed in patients undergoing hemodialysis. Key Words: endothelium Ⅲ far infrared therapy Ⅲ inflammation Ⅲ leukocyte adhesion A well-functioning vascular access is necessary for achieving adequate hemodialysis (HD) in patients with end stage renal failure. Approximately 17% to 25% of HD patient hospitalizations in the United States arise from vascular access complications, with an annual cost of more than 1 billion US dollars, which continues to grow. 1 Nearly 85% of vascular access failures arise from thromboses, more than 80% of which are associated with stenoses, 2 which usually presents with inadequate blood flow. 3,4 The causative factors of vascular access stenosis include small diameter of artery and vein, surgical technique, previous venipunctures, hemodynamic stress, and the presence of accessory veins. 5 Moreover, many factors leading to endothelial dysfunction, such as oxidative stress, hyperhomocysteinemia, platelet activation, and inflammation are associated with arteriovenous fistula (AVF) failure. 5 The histological features of vascular access stenosis comprise vascular inflammation, intimal hyperplasia, and excessive accumulation of extracellular matrix. 5 Despite these findings, the cause of stenoses remains unknown in a significant proportion of HD patients. This interindividual variation may relate to differences in the genetic background that may influence susceptibility to vascular inflammation and neointima formation after endothelial and smooth muscle injury. 6,7 Consistent with this notion, AVF survival was reported to be associated with specific genetic polymorphisms of transforming growth factor (TGF)-␤1 8 and methylene tetrahydrofolate reductase. 9 In addition, we recently identified a length polymorphism in the heme oxygenase-1 (HO-1) gene that is associated with patency of AVFs. 10 HO-1 catalyzes the oxidative degradation of heme into equimolar amounts of biliverdin,...

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“…Causative factors include a small artery (Ͻ1.5 to 2 mm) and a small vein (Ͻ2.0 to 2.5 mm), surgical manipulation and less-than-ideal technique, previous venipunctures, the development of accessory veins that direct blood away from the primary venous drainage channel, hemodynamic stressors (see below), and a possible genetic predisposition to vasoconstriction and neointimal hyperplasia after endothelial and smooth muscle injury (18,19). It still is unclear whether vascular constriction, neointimal hyperplasia, or a combination of the two factors is responsible for the early maturation failure of native fistulae.…”

Section: Pathogenesis Of Avf and Ptfe Graft Failurementioning

confidence: 99%

Hemodialysis Vascular Access Dysfunction: A Cellular and Molecular Viewpoint

Roy-Chaudhury¹

2006

Journal of the American Society of Nephrology

171

281

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Hemodialysis vascular access dysfunction is a major cause of morbidity and hospitalization in the hemodialysis population. The major cause of hemodialysis vascular access dysfunction is venous stenosis as a result of neointimal hyperplasia. Despite the magnitude of the clinical problem, however, there has been a paucity of novel therapeutic interventions in this field. This is in marked contrast to a recent plethora of targeted interventions for the treatment of arterial neointimal hyperplasia after coronary angioplasty. The reasons for this are two-fold. First there has been a relative lack of cellular and molecular research that focuses on venous neointimal hyperplasia in the specific setting of hemodialysis vascular access. Second, there have been inadequate efforts by the nephrology community to translate the recent advances in molecular and interventional cardiology into therapies for hemodialysis vascular access. This review therefore (1) briefly examines the different forms of hemodialysis vascular access that are available, (2) describes the pathology and pathogenesis of hemodialysis vascular access dysfunction in both polytetrafluoroethylene grafts and native arteriovenous fistulae, (3) reviews recent concepts about the pathogenesis of vascular stenosis that could potentially be applied in the setting of hemodialysis vascular access dysfunction, (4) summarizes novel experimental and clinical therapies that could potentially be used in the setting of hemodialysis vascular access dysfunction, and, finally, (5) offers some broad guidelines for future innovative translational and clinical research in this area that hopefully will reduce the huge clinical morbidity and economic costs that are associated with this condition.

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Is AV Fistula Patency Associated with Angiotensin-Converting Enzyme (ACE) Polymorphism and ACE Inhibitor Intake?

Cited by 29 publications

References 35 publications

The Presence of PAI-1 4G/5G and ACE DD Genotypes Increases the Risk of Early-Stage AVF Thrombosis in Hemodialysis Patients

The Presence of PAI-1 4G/5G and ACE DD Genotypes Increases the Risk of Early-Stage AVF Thrombosis in Hemodialysis Patients

Far Infrared Therapy Inhibits Vascular Endothelial Inflammation via the Induction of Heme Oxygenase-1

Hemodialysis Vascular Access Dysfunction: A Cellular and Molecular Viewpoint

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