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

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

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.

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

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

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

Full clinical history and through clinical examination. Full blood count at time of diagnosis and 3 months after initiation of treatment with iron and erythropoietin Stimulating agents. Iron study at time of diagnosis and 3 months after treatment . 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 .

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

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

if change of in Hemoglobin level and correction of anemia associated with change in the left ventricular outcomes

Inclusion Criteria: All patients: Above 18 years old Diagnosed as CKD, and renal transplanted patients at Assiut University Hospital in the period 2017-2020 . Exclusion Criteria: Severely hypocalcaemic patients < 7mg/dl. Severely hyperphosphatemic patients >7 mg/dl . Uncontrolled hypertensive patients ( more than 3 antihypertensive drugs). Uncontrolled diabetic patients HBA1C >8 . Blood transfusion dependent

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