NCT03193073

Anemia Correction and Fibroblast Growth Factor 23 Levels in Chronic Kidney Disease , and Renal Transplant Patient

Impact of Anemia Correction and Fibroblast Growth Factor 23 Levels in Left Ventricular Hypertrophy, and Early Endothelial Dysfunction in Chronic Kidney Disease, and Renal Transplant Patient

• Status: Suspended
• Phase: N/A
• Study type: Interventional
• Enrollment: 80 (estimated)
• Sponsor: Omnia Mohammed Hashem · Academic / Other
• Sex: All
• Age: 18 Years – 60 Years
• Healthy volunteers: Not accepted

Summary

The fibroblast growth factor-23-bone-kidney axis is part of newly discovered biological systems linking bone to other organ functions through a complex endocrine network that is integrated with the parathormone/vitamin D axis and which plays an equally important role in health and disease . Most of the known physiological function of fibroblast growth factor 23 to regulate mineral metabolism can be accounted for by actions of this hormone on the kidney.In a recent experimental study, fibroblast growth factor-23 was shown to cause pathological hypertrophy in rat cardiomyocytes by "calcineurin-nuclear factor of activated T cells" and treatment with fibroblast growth factor -blockers reduced left ventricular hypertrophy in experimental models of chronic renal failure.The current hypothesis is that, in healthy individuals, iron deficiency stimulates increased production of fibroblast growth factor23. At the same time, iron is thought to be the cofactor of enzymes taking part in the degradation of intact fibroblast growth factor-23 and thought to have a role in the excretion of degraded FGF-23 parts .Studies speculated that Angiotensin Converting Enzyme inhibitors may exert their anti-proteinuria effects at least in part by reducing serum fibroblast growth factor-23 levels although it is difficult from the results of this study to understand which comes first and brings about the other; decrease in proteinuria or fibroblast growth factor-23. Available evidence points to the deleterious effects of increased fibroblast growth factor-23 level in proteinuria, but the precise molecular mechanism still remains to be explored. An intricate and close association exists among parathormone, phosphorus, active vitamin D with FGF23, but the independent role of the latter on proteinuria is the least explored. Elaborately conducted studies that control effects of confounding factors adequately are needed to demonstrate the independent pathogenic role of FGF23.

Detailed description

1. To study the effect of anemia correction and left ventricular hypertrophy in Chronic Kidney Disease patients and renal transplant patients . 2. To study the relation of fibroblast growth factor and Left ventricular hypertrophy in Chronic kidney disease and renal transplant patients. 3. To study the relation between fibroblast growth factor 23 and early endothelial dysfunction in both Chronic kidney disease and renal transplant patients.

Conditions

• Anemia of Chronic Kidney Disease
• Endothelial Dysfunction
• Left Ventricular Hypertrophy
• Fibroblast Growth Factor 23

Interventions

Type	Name	Description
DIAGNOSTIC_TEST	detailed echocardiography	Detailed Echocardiography including ejection fraction, interventricular septum thickness, posterior wall thickness, left ventricular end -diastolic and end- systolic diameter and left ventricular mass index will be correlated with body surface area for both groups serum FGF-23
DIAGNOSTIC_TEST	serum fibroblast growth factor-23	serum levels of FGF-23
DIAGNOSTIC_TEST	flow mediated dilatation of forearm	superficial sonar assess the diameter of brachial vessel on exposure to stress

Timeline

• Start date: 2018-09-01
• Primary completion: 2020-09-01
• Completion: 2020-12-01
• First posted: 2017-06-20
• Last updated: 2018-06-27

Locations

1 site across 1 country: Egypt