The true cost of phosphate control in chronic kidney disease.

IF 3.9 2区 医学 Q1 UROLOGY & NEPHROLOGY Clinical Kidney Journal Pub Date : 2025-03-13 eCollection Date: 2025-03-01 DOI:10.1093/ckj/sfae434
Cristian Rodelo-Haad, María E Rodríguez-Ortiz, Raquel Garcia-Sáez, Antonio Rivas-Domínguez, Daniel Jurado-Montoya, Alejandro Martín-Malo, Mariano Rodríguez, M Victoria Pendón-Ruiz de Mier, Juan Rafael Muñoz-Castañeda
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Abstract

The loss of kidney function entails the development of a positive phosphate balance. The burden of addressing elevated phosphate levels is high. Both parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) are increased to promote phosphaturia, thereby preventing the rise in serum phosphate. However, if the phosphate load is excessive, the corresponding phosphaturia is maximal, kidney function deteriorates and hyperphosphataemia becomes clinically evident in advanced stages of chronic kidney disease (CKD). In addition to its role in CKD progression, hyperphosphataemia has been linked to a multitude of adverse outcomes, including overt inflammation, vascular calcifications, endothelial dysfunction, cardiovascular disease, renal osteodystrophy and secondary hyperparathyroidism. Collectively, these factors contribute to the markedly elevated mortality rates observed among individuals with CKD. Furthermore, hyperphosphataemia has been identified as a significant contributor to the development of inflammatory processes, oxidative stress and fibrosis, which underlie the aetiology of numerous comorbidities. Additionally, elevated levels of PTH and FGF23 have been demonstrated to independently induce organ and tissue injury, which is associated with poor outcomes in CKD. This article provides a concise overview of the current understanding of phosphate handling by the kidney in the context of CKD. It outlines the detrimental effects of phosphate on various organs and the mechanisms through which it contributes to CKD progression. Additionally, we discuss the tools available for clinicians to identify patients at risk of an excessive phosphate load.

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来源期刊
Clinical Kidney Journal
Clinical Kidney Journal Medicine-Transplantation
CiteScore
6.70
自引率
10.90%
发文量
242
审稿时长
8 weeks
期刊介绍: About the Journal Clinical Kidney Journal: Clinical and Translational Nephrology (ckj), an official journal of the ERA-EDTA (European Renal Association-European Dialysis and Transplant Association), is a fully open access, online only journal publishing bimonthly. The journal is an essential educational and training resource integrating clinical, translational and educational research into clinical practice. ckj aims to contribute to a translational research culture among nephrologists and kidney pathologists that helps close the gap between basic researchers and practicing clinicians and promote sorely needed innovation in the Nephrology field. All research articles in this journal have undergone peer review.
期刊最新文献
New perspectives on chronic kidney disease-mineral bone disorder. Pathophysiology and therapies of CKD-associated secondary hyperparathyroidism. Pathophysiology of chronic kidney disease-mineral bone disorder (CKD-MBD): from adaptive to maladaptive mineral homeostasis. The true cost of phosphate control in chronic kidney disease. Valvular calcification in chronic kidney disease: new insights from recent clinical and preclinical studies.
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