Working...
ClinicalTrials.gov
ClinicalTrials.gov Menu

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

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
ClinicalTrials.gov Identifier: NCT03193073
Recruitment Status : Suspended (problem in funding which will be solved by the end of August)
First Posted : June 20, 2017
Last Update Posted : June 27, 2018
Sponsor:
Information provided by (Responsible Party):
Omnia Mohammed Hashem, Assiut University

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.

Condition or disease Intervention/treatment Phase
Anemia of Chronic Kidney Disease Endothelial Dysfunction Left Ventricular Hypertrophy Fibroblast Growth Factor 23 Diagnostic Test: detailed echocardiography Diagnostic Test: serum fibroblast growth factor-23 Diagnostic Test: flow mediated dilatation of forearm Not Applicable

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.

Layout table for study information
Study Type : Interventional  (Clinical Trial)
Estimated Enrollment : 80 participants
Allocation: Randomized
Intervention Model: Parallel Assignment
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

Masking: None (Open Label)
Primary Purpose: Diagnostic
Official Title: 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
Estimated Study Start Date : September 1, 2018
Estimated Primary Completion Date : September 1, 2020
Estimated Study Completion Date : December 1, 2020

Resource links provided by the National Library of Medicine


Arm Intervention/treatment
Active Comparator: CKD patients with different stages
  1. Full clinical history and through clinical examination.
  2. Full blood count at time of diagnosis and 3 months after initiation of treatment with iron and erythropoietin Stimulating agents.
  3. Iron study at time of diagnosis and 3 months after treatment .
  4. Serum calcium , phosphorus, intact Parathrmone hormone. 5-24- urinary proteins or Albumin Creatinine ratio every month (for 3 months )then every 3 months (1 st year), then annually.

6- Lipid profile . 7-Estimated glomerular filtration rate by MDRD equation .

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

Active Comparator: Newly renal transplanted patients .
  1. Full clinical history and through clinical examination.
  2. Pre transplant Serum calcium , phosphorus , I Parathrmone hormone , serial measures every / 3 months for 2 years.
  3. Pre-transplant full blood count serial measures every / 3 months for 2 years.
  4. Pre transplant serum Iron study and annually for 2 years.
  5. 24- urinary proteins or albumin-creatinine ratio every month (for 3 months )then every 3 months (1 st year), then annually.
  6. Post-transplant serum FGF-23 (as independent risk factor) at 6months.
  7. Different immunosuppressive protocols.
  8. Pre-transplant panel reactive antibody,donor-specific antibody
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




Primary Outcome Measures :
  1. if change of in Hemoglobin level and correction of anemia associated with change in the left ventricular outcomes [ Time Frame: measures at time of diagnosis then after 3 months ]
    measure the left ventricular mass index (gm/m2)

  2. the relationship between the FGF-23 and degree of left ventricular dysfunction [ Time Frame: measure at time of diagnosis ]
    measure FGF-23 level in (pg/ml)

  3. the relationship between FGF-23 level and early endothelial dysfunction [ Time Frame: at time of diagnosis in chronic kidney disease / after 6 months in renal transplant ]
    change in arterial diameter in mm



Information from the National Library of Medicine

Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies.


Layout table for eligibility information
Ages Eligible for Study:   18 Years to 60 Years   (Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Criteria

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

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT03193073


Locations
Layout table for location information
Egypt
Assiut University Hospitals
Assiut, Egypt
Sponsors and Collaborators
Omnia Mohammed Hashem
Investigators
Layout table for investigator information
Study Director: Mohammed Ali Tohamy, professor Assiut University

Publications of Results:

Layout table for additonal information
Responsible Party: Omnia Mohammed Hashem, Assistant lecturer at Assiuy university- faculty of medicine-internal medicine department, Assiut University
ClinicalTrials.gov Identifier: NCT03193073     History of Changes
Other Study ID Numbers: 17200031
First Posted: June 20, 2017    Key Record Dates
Last Update Posted: June 27, 2018
Last Verified: June 2018
Individual Participant Data (IPD) Sharing Statement:
Plan to Share IPD: Undecided

Layout table for additional information
Studies a U.S. FDA-regulated Drug Product: No
Studies a U.S. FDA-regulated Device Product: No

Additional relevant MeSH terms:
Layout table for MeSH terms
Kidney Diseases
Renal Insufficiency, Chronic
Hypertrophy, Left Ventricular
Anemia
Hypertrophy
Hematologic Diseases
Urologic Diseases
Renal Insufficiency
Pathological Conditions, Anatomical
Cardiomegaly
Heart Diseases
Cardiovascular Diseases
Mitogens
Mitosis Modulators
Molecular Mechanisms of Pharmacological Action