Anemia of Chronic Kidney Disease, Endothelial Dysfunction, Fibroblast Growth Factor 23, Left Ventricular Hypertrophy
Conditions
Brief 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.
Interventions
DIAGNOSTIC_TESTdetailed 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_TESTserum fibroblast growth factor-23
serum levels of FGF-23
DIAGNOSTIC_TESTflow mediated dilatation of forearm
superficial sonar assess the diameter of brachial vessel on exposure to stress
Sponsors
Omnia Mohammed Hashem
Study design
Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
DIAGNOSTIC
Masking
NONE
Intervention model description
two groups of patients (group A: CKD and group B newly transplanted patients) are assigned for detailed echocardiography , serum FGF-23, flow mediated dilatation of the forearm before anaemia correction in group A and renal transplant in group B . Also assesment of FGF-23 in different stages of group A, assessment of FGF-23 before and after renal transplant
Eligibility
Sex/Gender
ALL
Age
18 Years to 60 Years
Healthy volunteers
No
Inclusion criteria
All patients: 1. Above 18 years old 2. Diagnosed as CKD, and renal transplanted patients at Assiut University Hospital in the period 2017-2020 .
Exclusion criteria
1. Severely hypocalcaemic patients \< 7mg/dl. 2. Severely hyperphosphatemic patients \>7 mg/dl . 3. Uncontrolled hypertensive patients ( more than 3 antihypertensive drugs). 4. Uncontrolled diabetic patients HBA1C \>8 . 5. Blood transfusion dependent
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| if change of in Hemoglobin level and correction of anemia associated with change in the left ventricular outcomes | measures at time of diagnosis then after 3 months | measure the left ventricular mass index (gm/m2) |
| the relationship between the FGF-23 and degree of left ventricular dysfunction | measure at time of diagnosis | measure FGF-23 level in (pg/ml) |
| the relationship between FGF-23 level and early endothelial dysfunction | at time of diagnosis in chronic kidney disease / after 6 months in renal transplant | change in arterial diameter in mm |
Countries
Egypt
Outcome results
None listed