Clinical Trial Details
— Status: Not yet recruiting
Administrative data
| NCT number |
NCT05854576 |
| Other study ID # |
mineral metabolism in ESRD |
| Secondary ID |
|
| Status |
Not yet recruiting |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
September 1, 2023 |
| Est. completion date |
November 1, 2024 |
Study information
| Verified date |
May 2023 |
| Source |
Assiut University |
| Contact |
soad elsayed |
| Phone |
011193711 |
| Email |
asoad381[@]gmail.com |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
Aim of the study is to determine the association of markers of mineral metabolism with
vascular access out come (maturation, patency of vascular access[AVF,AVG])To verify the
relationship between vascular access complication (AVF,AVG) and lower levels of 25(OH)D,
higher levels of fibroblast growth factor 23 (FGF23) and serum calcium, phosphorus,
parathyroid hormone (PTH) in patients with ESRD on regular hemodialysis.
Description:
Maintaining patent vascular access is essential for patients with end-stage renal disease
(ESRD) on hemodialysis (HD) to prevent life-threatening technique failure. Access
complications result in a high burden of hospital admissions, procedures, and costs for
patients on HD.
, The pathophysiologic mechanisms underlying vascular access complications are poorly
understood. Discovery of potential predictors and subsequent targets for intervention could
help design new preventive strategies.Abnormalities in mineral homeostasis are common in
patients with ESRD and are associated with numerous adverse outcomes including vascular
calcification, inflammation, and mortality.
The Klotho gene encodes for a transmembrane protein, acting as a co-receptor for fibroblast
growth factor-23 (FGF23) . The main functions of FGF23 signaling in the kidney are the
suppression of vitamin D hormone synthesis, and the suppression of renal tubular phosphate
reabsorption .
Impaired excretion of phosphorus due to low kidney function raises fibroblast growth factor
23 (FGF23). FGF23 decreases conversion of 25-hydroxy vitamin D (25(OH)D) to its active 1,25D
form, causing calcium to fall and parathyroid hormone(PTH) to rise The development of
secondary hyperparathyroidism lead to increased calcium and phosphate release from bones to
the blood, causing the deposition of calcium and phosphate in the intima-media layer of
arterial wall. and eventuating vascular calcification in these patients. the calcifications
might be encountered in the upper extremity arteries in cases with ESRD .Thus, a decrease in
the quality of fistula occurs in these tracts utilized frequently at the arteriovenous
fistula (AVF) operations. Thes complex interplay of factors may promote vascular disease
through multiple pathways including calcification, endothelial dysfunction, inflammation,
activation of the renin-angiotensin-aldosterone system and others are involved. Deficiency of
25(OH)D among patients with ESRD is above 80%.1,25D or its analogs are frequently
administered to patients with ESRD to overcome the adverse effects. low 25(OH)D associates
with mortality in HD patients.
Vitamin D deficiency has been associated with hypertension, insulin resistance, viral and
bacterial infection risk, and multiple organ damage due to systemic inflammation.
Despite consistent associations of disordered mineral homeostasis and vascular outcomes in
ESRD, few studies have investigated the role of these factors in vascular access out comes
