Why is homocysteine elevated in renal failure and what can be expected from homocysteine-lowering?

Guldener, Coen van

doi:10.1093/ndt/gfl044

Cited by 120 publications

(106 citation statements)

References 39 publications

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“…We demonstrate that coronary endothelial dysfunction is already apparent in mild to moderate CKD, which endorses the recent findings that the risk for cardiovascular events is already high in patients with kidney disease and microalbuminuria (4). In this regard, CKD is characterized by hyperhomocysteinemia in humans (34). Because our study failed to show a significant elevation in homocysteine levels, our canine model may not completely reflect the situation in humans with CKD.…”

Section: Discussionsupporting

confidence: 53%

Role of Nitric Oxide–Producing and–Degrading Pathways in Coronary Endothelial Dysfunction in Chronic Kidney Disease

Tatematsu¹,

Wakino²,

Kanda³

et al. 2007

Journal of the American Society of Nephrology

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Section: Discussionsupporting

confidence: 53%

Role of Nitric Oxide–Producing and–Degrading Pathways in Coronary Endothelial Dysfunction in Chronic Kidney Disease

Tatematsu¹,

Wakino²,

Kanda³

et al. 2007

Journal of the American Society of Nephrology

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“…For example, alterations in remethylation pathways and disturbance in cysteine disposal might also be impaired in patients with CKD. 9 The net consequences of elevated homocysteine levels may in turn be enhanced risk for the development of atherosclerosis. Although recent clinical trials aimed at lowering homocysteine levels have been disappointing, a preponderance of genetic and biochemical data suggest that elevated homocysteine levels promote a proatherogenic phenotype, with potential mechanisms including enhanced oxidative stress, inflammation, thrombosis, and endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Emerging Cardiovascular Risk Factors That Account for a Significant Portion of Attributable Mortality Risk in Chronic Kidney Disease

Shishehbor

Oliveira

Lauer

et al. 2008

The American Journal of Cardiology

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Chronic kidney disease (CKD) increases cardiovascular risk and mortality. However, traditional cardiovascular risk factors do not adequately account for the substantial increase in mortality observed in CKD. The aim of this study was to examine the relative contributions of novel cardiovascular risk factors to the risk between CKD and mortality. The study population included 4,680 consecutive new patients from a tertiary care preventive cardiology program from 1996 to 2005. Estimated glomerular filtration rate was calculated using the Modification of Diet in Renal Disease (MDRD) method. Baseline levels of traditional (low-density lipoprotein cholesterol, highdensity lipoprotein cholesterol, hypertension, triglycerides, total cholesterol, and fasting glucose) and emerging (apolipoproteins A-I and B, lipoprotein [a], fibrinogen, homocysteine, and highsensitivity C-reactive protein) risk factors were examined. All-cause mortality was obtained from the Social Security Death Index. There were 278 deaths over a median follow-up period of 22 months. CKD (estimated glomerular filtration rate ≤60 ml/min/1.73 m 2 ) was strongly associated with mortality after adjusting for traditional cardiovascular risk factors (hazard ratio 2.31, 95% confidence interval 1.77 to 3.11, p <0.001) and with the addition of propensity score (hazard ratio 2.33, 95% confidence interval 1.75 to 3.10, p <0.001). Of all the traditional and emerging risk factors monitored, only the addition of homocysteine and fibrinogen significantly attenuated the association between CKD and mortality (adjusted hazard ratio 1.73, 95% confidence interval 1.23 to 2.34, p <0.001), explaining 38% of the attributable mortality risk from CKD. A significant interaction (p = 0.004) between homocysteine and estimated glomerular filtration rate was observed whereby the annual mortality rate in subjects with CKD with homocysteine <10 μmol/L (the bottom tertile) was similar to those with normal renal function (1% per year), whereas homocysteine levels ≥12.5 μmol/L (the top tertile) were associated with a sevenfold greater mortality risk. In conclusion, homocysteine and fibrinogen levels explain nearly 40% of the attributable mortality risk from CKD. MethodsThe population consisted of consecutive new patients seen at a tertiary preventive cardiology program from 1996 to 2005. This population constituted primary and secondary cardiovascular prevention. Generally, all staff members within the preventive cardiology section follow a similar algorithm when treating risk factors such as hypertension, hyperlipidemia, obesity, glucose intolerance, and others. Patients were excluded if they lacked a United States Social Security number. In addition, we excluded individuals with end-stage renal disease requiring maintenance hemodialysis at baseline. Of a total of 5,636 new subjects seen, 4,680 had baseline laboratory data available. The Institutional Review Board of the Cleveland Clinic approved this study.All patients underwent detailed interviews by professional nursing staf...

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“…Además, la homocisteína inhibe la óxido nítrico sintetasa, potenciando la disfunción endotelial. Otros mecanismos pro aterogénicos de la hiperhomocisteinemia incluyen metilación desregulada de proteínas y ADN, induciendo proliferación anormal del músculo liso de la vasculatura, y peroxidación lipídica aumentada 8 .…”

Section: Introductionunclassified

“…Estando la hiperhomocisteinemia asociada a riesgo cardiovascular y mortalidad, reducir sus niveles suplementando folato podría ser un recurso terapéutico 8,9 .…”

Section: Introductionunclassified

Analisis crítico de dos revisiones sistemáticas: ¿Es útil el ácido fólico para prevenir eventos cardiovasculares en pacientes con enfermedad renal crónica terminal o avanzada?

Peña

Claro

2014

Rev. méd. Chile

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Why is homocysteine elevated in renal failure and what can be expected from homocysteine-lowering?

Cited by 120 publications

References 39 publications

Role of Nitric Oxide–Producing and–Degrading Pathways in Coronary Endothelial Dysfunction in Chronic Kidney Disease

Role of Nitric Oxide–Producing and–Degrading Pathways in Coronary Endothelial Dysfunction in Chronic Kidney Disease

Emerging Cardiovascular Risk Factors That Account for a Significant Portion of Attributable Mortality Risk in Chronic Kidney Disease

Analisis crítico de dos revisiones sistemáticas: ¿Es útil el ácido fólico para prevenir eventos cardiovasculares en pacientes con enfermedad renal crónica terminal o avanzada?

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