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The challenge of controlling phosphorus in chronic kidney disease.
Nephrol Dial Transplant. 2016 04; 31(4):541-7.ND

Abstract

The pathogenesis and management of chronic kidney disease-mineral bone disorders (CKD-MBD) has experienced major changes, but the control of serum phosphorus at all stages of CKD still seems to be a key factor to improve clinical outcomes. High serum phosphorus is the most important uremia-related, non-traditional risk factor associated with vascular calcification in CKD patients and in the general population. Phosphorus may also be one of the key elements linking vascular calcification with low bone turnover. The main hormones and factors that contribute to the kidney regulation of phosphorus and calcium include parathyroid hormone, FGF-23, klotho and 1,25-dihydroxyvitamin D (1,25(OH)2D). Serum phosphorus did not start rising until CKD 3b in contrast with the earlier changes observed with fibroblast growth factor-23 (FGF-23), Klotho, calcitriol and parathyroid hormone (PTH). Despite FGF-23 and PTH having synergic effects regarding phosphorus removal, they have opposite effects on 1,25(OH)2D3. At the same stages of CKD in which phosphorus retention appears to occur, calcium retention also occurs. As phosphorus accumulation is associated with poor outcomes, an important question without a clear answer is at which level-range should serum phosphorus be maintained at different stages of CKD to improve clinical outcomes. There are four main strategies to manage phosphate homeostasis; phosphorus dietary intake, administration of phosphate binder agents, effective control of hyperparathyroidism and to ensure in the CKD 5D setting, an adequate scheme of dialysis. Despite all the available strategies, and the introduction of new phosphate binder agents in the market, controlling serum phosphorus remains challenging, and hyperphosphatemia continues to be extremely common in CKD 5 patients. Furthermore, despite phosphate binding agents having proved to be effective in reducing serum phosphorus, their ultimate effects on clinical outcomes remain controversial. Thus, we still need well-designed, large-scale, placebo-controlled studies to definitively prove that the reduction of serum phosphorus by phosphate binders improves clinical outcomes.

Authors+Show Affiliations

Bone and Mineral Research Unit, Hospital Universitario Central de Asturias, Instituto Reina Sofía de Investigación, REDinREN del ISCIII, University of Oviedo, Asturias, Spain.Division of Nephrology, Saint Louis University School of Medicine, St. Louis, MO, USA.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

25770169

Citation

Cannata-Andía, Jorge B., and Kevin J. Martin. "The Challenge of Controlling Phosphorus in Chronic Kidney Disease." Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association, vol. 31, no. 4, 2016, pp. 541-7.
Cannata-Andía JB, Martin KJ. The challenge of controlling phosphorus in chronic kidney disease. Nephrol Dial Transplant. 2016;31(4):541-7.
Cannata-Andía, J. B., & Martin, K. J. (2016). The challenge of controlling phosphorus in chronic kidney disease. Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association, 31(4), 541-7. https://doi.org/10.1093/ndt/gfv055
Cannata-Andía JB, Martin KJ. The Challenge of Controlling Phosphorus in Chronic Kidney Disease. Nephrol Dial Transplant. 2016;31(4):541-7. PubMed PMID: 25770169.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The challenge of controlling phosphorus in chronic kidney disease. AU - Cannata-Andía,Jorge B, AU - Martin,Kevin J, Y1 - 2015/03/13/ PY - 2014/11/26/received PY - 2015/01/30/accepted PY - 2015/3/15/entrez PY - 2015/3/15/pubmed PY - 2017/7/19/medline KW - chronic kidney disease KW - clinical management KW - hyperphosphatemia KW - phosphate control SP - 541 EP - 7 JF - Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association JO - Nephrol Dial Transplant VL - 31 IS - 4 N2 - The pathogenesis and management of chronic kidney disease-mineral bone disorders (CKD-MBD) has experienced major changes, but the control of serum phosphorus at all stages of CKD still seems to be a key factor to improve clinical outcomes. High serum phosphorus is the most important uremia-related, non-traditional risk factor associated with vascular calcification in CKD patients and in the general population. Phosphorus may also be one of the key elements linking vascular calcification with low bone turnover. The main hormones and factors that contribute to the kidney regulation of phosphorus and calcium include parathyroid hormone, FGF-23, klotho and 1,25-dihydroxyvitamin D (1,25(OH)2D). Serum phosphorus did not start rising until CKD 3b in contrast with the earlier changes observed with fibroblast growth factor-23 (FGF-23), Klotho, calcitriol and parathyroid hormone (PTH). Despite FGF-23 and PTH having synergic effects regarding phosphorus removal, they have opposite effects on 1,25(OH)2D3. At the same stages of CKD in which phosphorus retention appears to occur, calcium retention also occurs. As phosphorus accumulation is associated with poor outcomes, an important question without a clear answer is at which level-range should serum phosphorus be maintained at different stages of CKD to improve clinical outcomes. There are four main strategies to manage phosphate homeostasis; phosphorus dietary intake, administration of phosphate binder agents, effective control of hyperparathyroidism and to ensure in the CKD 5D setting, an adequate scheme of dialysis. Despite all the available strategies, and the introduction of new phosphate binder agents in the market, controlling serum phosphorus remains challenging, and hyperphosphatemia continues to be extremely common in CKD 5 patients. Furthermore, despite phosphate binding agents having proved to be effective in reducing serum phosphorus, their ultimate effects on clinical outcomes remain controversial. Thus, we still need well-designed, large-scale, placebo-controlled studies to definitively prove that the reduction of serum phosphorus by phosphate binders improves clinical outcomes. SN - 1460-2385 UR - https://www.unboundmedicine.com/medline/citation/25770169/The_challenge_of_controlling_phosphorus_in_chronic_kidney_disease_ L2 - https://academic.oup.com/ndt/article-lookup/doi/10.1093/ndt/gfv055 DB - PRIME DP - Unbound Medicine ER -