Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Jan;108(1):116-127.
doi: 10.1007/s00223-020-00665-8. Epub 2020 Jan 29.

Hyperphosphatemia and Chronic Kidney Disease: A Major Daily Concern Both in Adults and in Children

Affiliations
Review

Hyperphosphatemia and Chronic Kidney Disease: A Major Daily Concern Both in Adults and in Children

Justine Bacchetta et al. Calcif Tissue Int. 2021 Jan.

Abstract

Hyperphosphatemia is common in chronic kidney disease (CKD). Often seen as the "silent killer" because of its dramatic effect on vascular calcifications, hyperphosphatemia explains, at least partly, the onset of the complex mineral and bone disorders associated with CKD (CKD-MBD), together with hypocalcemia and decreased 1-25(OH)2 vitamin D levels. The impact of CKD-MBD may be immediate with abnormalities of bone and mineral metabolism with secondary hyperparathyroidism and increased FGF23 levels, or delayed with poor growth, bone deformities, fractures, and vascular calcifications, leading to increased morbidity and mortality. The global management of CKD-MBD has been detailed in international guidelines for adults and children, however, with difficulties to obtain an agreement on the ideal PTH targets. The clinical management of hyperphosphatemia is a daily challenge for nephrologists and pediatric nephrologists, notably because of the phosphate overload in occidental diets that is mainly due to the phosphate "hidden" in food additives. The management begins with a dietary restriction of phosphate intake, and is followed by the use of calcium-based and non-calcium-based phosphate binders, and/or the intensification of dialysis. The objective of this review is to provide an overview of the pathophysiology of hyperphosphatemia in CKD, with a focus on its deleterious effects and a description of the clinical management of hyperphosphatemia in a more global setting of CKD-MBD.

Keywords: CKD–MBD; Calcium; Dialysis; FGF23; Osteodystrophy; PTH; Phosphate; Vascular calcifications; Vitamin D.

PubMed Disclaimer

References

    1. Mitsnefes MM (2012) Cardiovascular disease in children with chronic kidney disease. J Am Soc Nephrol 23(4):578–585 - PubMed - PMC - DOI
    1. Shroff R (2013) Phosphate is a vascular toxin. Pediatr Nephrol 28(4):583–593 - PubMed - DOI - PMC
    1. Shroff R, Long DA, Shanahan C (2013) Mechanistic insights into vascular calcification in CKD. J Am Soc Nephrol 24(2):179–189 - PubMed - DOI - PMC
    1. Moe S, Drüeke T, Cunningham J, Goodman W, Martin K, Olgaard K et al (2006) Definition, evaluation, and classification of renal osteodystrophy: a position statement from kidney disease: improving global outcomes (KDIGO). Kidney Int. 69(11):1945–1953 - PubMed - DOI - PMC
    1. Goodman WG, Goldin J, Kuizon BD, Yoon C, Gales B, Sider D et al (2000) Coronary-artery calcification in young adults with end-stage renal disease who are undergoing dialysis. N Engl J Med. 342(20):1478–1483 - PubMed - DOI - PMC

LinkOut - more resources