Homocysteine in uremia

Perna, Alessandra F.; Ingrosso, Diego; Lombardi, Cinzia; Cesare, Concetta Maria; Acantora, Filomena; Satta, Ersilia; Santo, Natale G. De

doi:10.1053/ajkd.2003.50100

Cited by 11 publications

(7 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…HHcy is an independent cardiovascular risk factor that possibly accounts for about one out of five cardiovascular deaths (9). HHcy has been reported to occur in 11-22% of westernised populations (10).…”

Section: Discussionmentioning

confidence: 99%

Plasma levels of homocysteine in patients with white-coat hypertension

Çoban

Özdoğan

Ermis

2004

International Journal of Clinical Practice

View full text Add to dashboard Cite

Elevated levels of plasma homocysteine (Hcy) is an independent risk factor for cardiovascular diseases. The risk profile of white-coat hypertension (WCHT) is not yet completely clear. In this study, we aim to determine the levels of plasma Hcy in a group of patients with WCHT, and to obtain clinical results by comparing WCHT group with hypertensive and healthy groups. Age, sex and body mass index were matched for 15 normal subjects, 15 patients with WCHT and 15 patients with essential hypertension, and they were included in the study. We measured levels of plasma Hcy in all groups. Levels of plasma Hcy were significantly higher in patients with sustained hypertension than in WCHT group (p = 0.03). They were also significantly higher in patients with WCHT than in control group (p = 0.02). Our data suggest that WCHT subjects are at an increased cardiovascular risk, although this was lower than the risk in patients with sustained hypertension.

show abstract

Section: Discussionmentioning

confidence: 99%

Plasma levels of homocysteine in patients with white-coat hypertension

Çoban

Özdoğan

Ermis

2004

International Journal of Clinical Practice

View full text Add to dashboard Cite

show abstract

“…Exogenous creatine supplementation can, thus, be expected to decrease endogenous Hcy synthesis. Inhibition of the methyltransferase reactions has been described in uremia due to a reduced S-adenosylmethionine (SAM)/S-adenosylhomocysteine (SAH) ratio, and protein hypomethylation and reduced protein repair are observed in uremic subjects [10,11]. The influence of creatine on tHcy concentrations, SAM/SAH ratios, and the methyltransferase reactions in humans is currently unknown.…”

mentioning

confidence: 99%

Creatine supplementation does not decrease total plasma homocysteine in chronic hemodialysis patients

Taes¹,

Delanghe²,

Bacquer³

et al. 2004

Kidney International

View full text Add to dashboard Cite

show abstract

“…On the basis of experimental data, homocysteine has been proposed to have a direct toxic effect on the endothelium, besides exerting a prothrombotic effect and increasing oxidative stress [11]. We were able to find increased systemic inflammation, assessed by the significant elevation of fibrinogen and hs-CRP, and a higher degree of endothelial damage as indicated by higher VWF levels in hyperhomocysteinemic RTRs.…”

mentioning

confidence: 66%

Folic acid and B vitamins improve hyperhomocysteinemia‐induced cardiovascular risk profile in renal transplant recipients

Manrique

Errasti

Orbe

et al. 2007

Journal of Thrombosis and Haemostasis

View full text Add to dashboard Cite

and reduction of tHcy by folic acid significantly decreases platelet activation.We extended previous findings demonstrating that enhanced platelet activation in the presence of elevated tHcy is detectable not only in vitro, but also in vivo at tHcy levels below 30 lmol L )1 when platelet activation is triggered by disruption of the blood vessel wall. No effect of tHcy on platelets in our model was found in the circulating venous blood. Decreasing platelet marker levels in shed blood after FA administration and correlations between the parameters of the platelet marker profiles and tHcy support the concept that in vivo homocysteine itself contributes to platelet hyperreactivity. In 1999, we demonstrated that in hyperhomocysteinemic subjects vitamin therapy is associated with decreased thrombin generation at the site of microvascular injury [9]. In the current study, using the same experimental approach, we provided evidence for platelet activation in hyperhomocysteinemic individuals and its attenuation as the FA-mediated effect. A model of microvascular injury can demonstrate an impact of various factors, including elevated tHcy, on the three major components of hemostasis, namely, circulating platelets, plasma coagulation proteins and the vessel wall.Profiles of both platelet markersÕ release in the current study were similar to those found in high-risk patients [9,10], although maximum levels and velocity of their increase were now lower, most likely as a result of the exclusion of subjects with a history of cardiovascular disease. Folic acid-related changes in these release profiles were subtle, although significant, which might suggest that in severe atherosclerosis or acute coronary syndromes, antiplatelet effects of vitamins could be overcome by the generation of other potent platelet agonists such as thrombin.In conclusion, we suggest that mild hyperhomocysteinemia may promote platelet activation induced by vascular injury in asymptomatic individuals and this effect can be abolished by FA. Whether similar observations can be made in patients with documented cardiovascular disease is under investigation. Disclosure of Conflict of InterestsThe authors state that they have no conflict of interest. Cardiovascular disease (CVD) is the single most common cause of death in renal transplant recipients (RTRs), accounting for 35-50% of all-cause mortality, and CVD mortality rates are at least twice as high as in an age-stratified sample of the general population [1]. The increased incidence of established cardiovascular risk factors, especially hypertension, diabetes and dyslipidemia, in RTRs may account, at least in part, for their Correspondence: Jose´A. Rodrı´guez,

show abstract

Homocysteine in uremia

Cited by 11 publications

References 20 publications

Plasma levels of homocysteine in patients with white-coat hypertension

Plasma levels of homocysteine in patients with white-coat hypertension

Creatine supplementation does not decrease total plasma homocysteine in chronic hemodialysis patients

Folic acid and B vitamins improve hyperhomocysteinemia‐induced cardiovascular risk profile in renal transplant recipients

Contact Info

Product

Resources

About