Phosphorous metabolism and manipulation in chronic kidney disease
Informazioni aggiuntive
Autori
Marando M.,
Tamburello A.,
Salera D.,
Di Lullo L.,
Bellasi A.
Tipo
Articolo pubblicato in rivista scientifica
Anno
2024
Lingua
Inglese
Sommario
Chronic kidney disease-mineral bone disorder (CKD-MBD) is a syndrome commonly observed in subjects with impaired renal function. Phosphate metabolism has been implicated in the pathogenesis of CKD-MBD and according to the phosphorocentric hypothesis may be the key player in the pathogenesis of these abnormalities. As phosphorous is an essential component for life, absorption from the bowel, accumulation and release from the bones, and elimination through the kidneys are all homeostatic mechanisms that maintain phosphate balance through very sophisticated feedback mechanisms, which comprise as main actors: vitamin D (VD), parathyroid hormone (PTH), calciproteins particles (CPPs), fibroblast growth factor-23 (FGF-23) and other phosphatonins and klotho. Indeed, as the renal function declines, factors such as FGF-23 and PTH prevent phosphate accumulation and hyperphosphatemia. However, these factors per se may be responsible for the organ damages associated with CKD-MBD, such as bone osteodystrophy and vascular calcification. We herein review the current understanding of the CKD-MBD focusing on phosphorous metabolism and the impact of phosphate manipulation on surrogate and hard outcomes.
Parole chiave
CKD, Dialysis, Outcome, Phosphate binders, Phosphorous
Periodico
Nephrology
Volume
29
Numero ( Mese )
12
Pagine (o numero dell’articolo)
791-800
Diffusione
Licenza
CC BY-NC-ND
Visibilità
Pubblico
Status open access
Hybrid
