Ignite Creation Date:
2025-12-24 @ 11:54 PM
Ignite Modification Date:
2026-03-06 @ 5:55 AM
Study NCT ID:
NCT03749551
Status:
COMPLETED
Last Update Posted:
2023-07-13
First Post:
2018-11-17
Is Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Towards Understanding the Phenotype of Cardiovascular Disease in CKD - TRUE-Type-CKD Study
Sponsor:
Johann Wolfgang Goethe University Hospital
Organization:
Study Overview
Official Title:
TowaRds Understanding the phEnoTYPEs of Cardiovascular Dysfunction in Patients With Chronic Kidney Disease and HaemoDialysis Using Cardiovascular Magnetic Resonance Imaging - TRUE-Type-CKD Study
Status:
COMPLETED
Status Verified Date:
2023-07
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
TRUE-TypeCKD
Brief Summary:
Premature cardiovascular disease (CVD) is the leading cause of death in patients with kidney disease (CKD). Excessive cardiac mortality is thought to be secondary to non-atherosclerotic processes, with left ventricular (LV) hypertrophy (LVH) and remodelling being the predominant phenotypical features. Along with other risk factors, subclinical ischaemia and haemodynamic perturbations associated with haemodialysis (HD) are thought to contribute to the ultimate development of LV systolic and diastolic dysfunction. The development of these adverse features reflects a specific cardiomyopathy due to CKD and subsequently, to uraemia. Patients receiving hemodialysis (HD) have a higher incidence rate of heart failure (predominantly with preserved ejection fraction), with phenotypically eccentric hypertrophic remodelling, systolic and diastolic dysfunction as well as high rate of interstitial myocardial fibrosis. Detection and ultimately reversal of the development of this CKD-related cardiomyopathy are important goals for improving the CVD, morbidity and mortality of CKD patients.The objectives of this study are, firstly, to investigate the complex myocardial phenotype in patients with various stages of CKD, secondly, to relate the CMR-measures to outcome, and thirdly, to be able to estimate the effects of chronic uremia/hypervolemia. Deciphering the predominant driver of remodelling on an individual level may help to personalise anti-remodelling strategies. Native T1 and T2 mapping imaging provide non-invasive imaging tools to detect myocardial fibrosis and oedema, respectively. Prognostic associations of these measures may clarify the relative prevalence of adverse phenotype and their relative contribution to adverse events and poor outcome. The role of chronic water retention and uraemia may be associated with interstitial myocardial oedema promoting further the remodelling process.
Detailed Description:
None
Study Oversight
Has Oversight DMC:
False
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?: