Fibrinogen, coagulation factor VII, tissue plasminogen activator, plasminogen activator inhibitor-1, and lipid as cardiovascular risk factors in chronic hemodialysis and continuous ambulatory peritoneal dialysis patients

Tomura, Shigeo; Nakamura, Yoshihiro; Doi, Mayumi; Ando, Ryoichi; Ida, Takashi; Chida, Yoshiko; Ootsuka, Shoichi; Shinoda, Takeshi; Yanagi, Hisako; Tsuchiya, Shigeru; Marumo, Fumiaki

doi:10.1016/s0272-6386(96)90523-5

Cited by 87 publications

(66 citation statements)

References 43 publications

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“…35 Stegnar et al studied 158 patients and 145 controls. They determined a relationship between 46-56 genotypes and deep vein thrombosis (DVT), but they obtained the same 46-56 genotype distribution in both groups.…”

Section: Discussionmentioning

confidence: 99%

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: 99%

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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“…The major finding is that endogenous bradykinin contributes to increased MCP-1 and PAI-1 concentrations after hemodialysis via a B 2 -receptor dependent mechanism. Given that PAI-1 antigen and activity independently predict cardiovascular mortality and thrombotic events in CHD patients, 10,11,28 the data suggest that factors that increase the formation of bradykinin or decrease its degradation would increase cardiovascular risk in the CHD population.…”

Section: Discussionmentioning

confidence: 99%

Endogenous Bradykinin Contributes to Increased Plasminogen Activator Inhibitor 1 Antigen following Hemodialysis

Marney¹,

Ma²,

Luther

et al. 2009

Journal of the American Society of Nephrology

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Oxidative stress and inflammation predict cardiovascular events in chronic hemodialysis patients. Hemodialysis activates the kallikrein-kinin system, increasing bradykinin. Bradykinin promotes inflammation but also stimulates endothelial release of tissue-plasminogen activator and inhibits platelet aggregation. Understanding the detrimental and beneficial effects of endogenous bradykinin during hemodialysis has implications for the treatment of cardiovascular disease in the hemodialysis population. To test the hypothesis that bradykinin contributes to the inflammatory and fibrinolytic responses to dialysis, we conducted a double-blind, randomized, placebo-controlled crossover study comparing the effect of the bradykinin B 2 receptor blocker HOE-140 with vehicle on markers of oxidative stress, inflammation, fibrinolysis, and coagulation in nine hemodialysis patients without coronary artery disease. Bradykinin receptor antagonism did not affect the mean arterial pressure or heart rate response to dialysis. Monocyte chemoattractant protein 1 (MCP-1) peaked postdialysis; HOE-140 blunted the increase in MCP-1 (5.9 Ϯ 5.9 versus 25.6 Ϯ 20.1 pg/ml, P ϭ 0.01). HOE-140 also abolished the increase in plasminogen activator inhibitor 1 (PAI-1) antigen observed at the end of dialysis. In contrast, HOE-140 significantly accentuated the effect of dialysis on F 2 -isoprostanes and P-selectin. Taken together, these results suggest that endogenous bradykinin contributes to increases in MCP-1 and PAI-1 antigen after hemodialysis via its B 2 receptor. Factors that increase the production of bradykinin or decrease its degradation may enhance the inflammatory response to hemodialysis.

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“…37 Second, patients with CKD without AF is associated with a prothrombotic state, including endothelial damage, alteration in protein C metabolism, defects in the expression of glycoprotein Ib, elevated levels of various plasminogen activator inhibitor-1 and von Willebrand factor, abnormalities in various coagulation factor levels and activity, as well as inflammation. [38][39][40][41] Third, CKD is further associated with abnormality of neurohormonal (eg, renin-angiotensin-aldosterone system), inflammatory, and oxidative pathways or mineral metabolism (eg, hyperparathyroidism), which may result in atherosclerosis and thus greater risk of thromboembolic events. 42 Therefore, CKD may contribute to an increased risk of ischemic stroke and other thromboembolism in AF patients by augmenting the underlying prothrombotic state through several different pathophysiological pathways.…”

Section: Zeng Et Al Ckd and Stroke Risk In Af 161mentioning

confidence: 99%

Risk of Thromboembolic Events in Atrial Fibrillation With Chronic Kidney Disease

Zeng

Sun

Tang

et al. 2015

Stroke

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Background and Purpose-Chronic kidney disease may increase the risk for ischemic stroke or systemic embolism in patients with nonvalular atrial fibrillation (AF). We conducted a meta-analysis to summarize all published studies to investigate the link between chronic kidney disease and risk of thromboembolic events in AF. Methods-We performed a literature search using MEDLINE (source PubMed, 1966 and EMBASE (1980 to July 2014) with no restrictions. Pooled effect estimates were obtained by using random-effects meta-analysis. Results-Eighteen studies involving 538 479 patients and 41 719 incident thromboembolic events were identified. From the pooled analysis, AF patients with estimated glomerular filtration rate <60 mL/min compared with those with estimated glomerular filtration rate ≥60 mL/min experienced a significantly increased risk for developing thromboembolic events (relative risk, 1.62 [95% confidence interval, 1.40-1.87; P<0.001]). The annual rate of thromboembolic events increased by 0.41% (95% confidence interval, 0.17%-0.65%) for a 10 mL/min decrease in renal function. Addition of renal impairment to CHADS 2 slightly improved the stroke risk stratification. Conclusions-Impaired renal function is an independent predictor of stroke or systemic embolism in patients with nonvalvular AF. Consideration of renal function may improve stroke risk stratification in patients with AF. (Stroke.

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Fibrinogen, coagulation factor VII, tissue plasminogen activator, plasminogen activator inhibitor-1, and lipid as cardiovascular risk factors in chronic hemodialysis and continuous ambulatory peritoneal dialysis patients

Cited by 87 publications

References 43 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

Endogenous Bradykinin Contributes to Increased Plasminogen Activator Inhibitor 1 Antigen following Hemodialysis

Risk of Thromboembolic Events in Atrial Fibrillation With Chronic Kidney Disease

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