Phosphorous metabolism and manipulation in chronic kidney disease

• Published in: Nephrology (Carlton, Vic.) Vol. 29; no. 12; pp. 791 - 800
• Main Authors: Marando, Marco, Tamburello, Adriana, Salera, Davide, Di Lullo, Luca, Bellasi, Antonio
• Format: Journal Article
• Language: English
• Published: Melbourne John Wiley & Sons Australia, Ltd 01.12.2024; Wiley Subscription Services, Inc
• Subjects: Animals; Calcification (ectopic); Chronic Kidney Disease-Mineral and Bone Disorder - etiology; Chronic Kidney Disease-Mineral and Bone Disorder - metabolism; CKD; dialysis; Fibroblast Growth Factor-23 - metabolism; Fibroblast growth factors; Fibroblast Growth Factors - metabolism; Humans; Hyperphosphatemia; Hyperphosphatemia - etiology; Hyperphosphatemia - metabolism; Kidney - metabolism; Kidney - physiopathology; Kidney diseases; Klotho protein; Metabolism; Osteodystrophy; outcome; Parathyroid hormone; Pathogenesis; phosphate binders; Phosphates - metabolism; phosphorous; Phosphorus - metabolism; Renal function; Renal Insufficiency, Chronic - complications; Renal Insufficiency, Chronic - metabolism; Review; Sexually transmitted diseases; STD; Vitamin D; dialysis; phosphate binders; CKD; phosphorous; outcome
• ISSN: 1320-5358; 1440-1797; 1440-1797
• DOI: 10.1111/nep.14407

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. Summary at glance Chronic kidney disease‐mineral bone disorder (CKD‐MBD) is commonly seen in individuals with impaired renal function. Phosphate balance is crucial, involving key factors like vitamin D, parathyroid hormone (PTH), calciprotein particles (CPPs) and fibroblast growth factor‐23 (FGF‐23). While these factors prevent phosphate accumulation, they may also contribute to organ damage. Efforts are needed to understand the impact of phosphate manipulation on outcomes in CKD‐MBD.