Methylation Biosignature in Childhood Chronic Kidney Disease

NCT02022046 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 69

Last updated 2017-07-21

No results posted yet for this study

Summary

Chronic kidney disease (CKD) and end-stage renal disease are highly prevalent in Taiwan. Cardiovascular disease (CVD) is the most common cause of death in children with CKD. Nitric oxide (NO) deficiency links CKD and CVD. Asymmetric dimethylarginine (ADMA), a NO synthase inhibitor, its level is increased in kidney disease and cardiovascular disease and serves as a methylation biomarker.

In addition to ADMA, uremic environment, hyperhomocysteinemia (Hcy) and oxidative stress may affect DNA methylation. S-adenosylmethionine (SAM) is an important human methyl donor. S-adenosylhomocysteine (SAH) is demethylated product. Methylenetetrahydrofolate reductase (MTHFR), a folate metabolism enzyme can regulate methylation pathway.

The investigators intend to examine whether ADMA, SAM/SAH ratio, Hcy, and MTHFR gene methylation can serve as biosignature to predict CVD in children with CKD children.

Conditions

Interventions

OTHER

Methylation biosignature

Methylation biosignature, CKD staging, assessment of cardiovascular function, and traditional/uremia-related risk factors will be performed.

Sponsors & Collaborators

  • Chang Gung Memorial Hospital

    lead OTHER

Principal Investigators

  • You-Lin Tain, MD, PhD · Chang Gung Memorial Hospital

Eligibility

Min Age
3 Years
Max Age
18 Years
Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2014-04-30
Primary Completion
2016-11-30
Completion
2016-12-31

Countries

  • Taiwan

Study Locations

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Entities

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT02022046 on ClinicalTrials.gov