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

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.

Conditions

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

Interventions

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

Sponsors & Collaborators

• Omnia Mohammed Hashem

  lead OTHER

Principal Investigators

• Mohammed Ali Tohamy, professor · Assiut University

Study Design

Allocation

RANDOMIZED

Purpose

DIAGNOSTIC

Masking

NONE

Model

PARALLEL

Eligibility

Min Age

18 Years

Max Age

60 Years

Sex

ALL

Healthy Volunteers

No

Timeline & Regulatory

Start

2018-09-01

Primary Completion

2020-09-01

Completion

2020-12-01

Countries

• Egypt

Study Locations