Biomarkers - FGF-23 and α-Klotho in hemodialysis patients with secondary hyperparathyroidism

Abstract

Chronic kidney disease has been shown to impair the metabolism of a number of minerals, resulting in bone damage, vascular wall calculations, functional disorders and significant mortality.

Renal osteodystrophy in this disease is characterized by histological bone abnormalities and altered rate of bone transformation (increased in fibrous osteitis or decreased in adynamic bone disease), pathological mineralization (osteomalacia) and bone loss. Secondary hyperparathyroidism is associated with fibrosis osteitis, early build-up of phosphorus (responsible for excess production of FGF23 by the bone tissue), decreased production of calcitriol by the kidneys and hypocalcemia. Other bone debilitating factors include acidosis, chronic inflammation, food deficiency, and iatrogenic complications.

It has been proven  that with the progression of CKD and the reduction of glomerular filtration, the activity of FGF-23 is increased, which leads to inhibition of alpha-1 hydroxylase and to decrease levels of 1,25 dihydroxyvitamin D. /1/

FGF-23 comes predominantly from the bones, while αKlotho - from the kidneys, and together they play different important roles to maintain mineral metabolism. Chronic kidney disease is associated with significant increases in FGF-23 concentrations and inhibition of αKlotho.

Hyperphosphatemia, which correlates with endothelial dysfunction and elevated FGF-23, in an untimely treatment, results in pruritus, bone pain, anemia, cardiovascular complications, disability, and reduced survival rate.

The association between protein-related uremic toxins and fibroblast growth factor-23  / FGF-23  is a challenge motivating the study and study of bone biomarkers.