Tags

Type your tag names separated by a space and hit enter

Phosphate: a stealthier killer than previously thought?
Cardiovasc Pathol. 2012 Sep-Oct; 21(5):372-81.CP

Abstract

The kidneys excrete excess dietary phosphate, and patients with chronic kidney disease may suffer from phosphate overload and hyperphosphatemia. In chronic kidney disease, hyperphosphatemia has emerged as a risk factor for vascular calcification, cardiovascular mortality, left ventricular hypertrophy, and progression of chronic kidney disease. Serum phosphate at the upper limits of normal has also been associated with adverse outcomes in patients with relatively preserved kidney function. Of note, hyperphosphatemia is not a sensitive indicator of phosphate overload. In this regard, increased circulating fibroblast growth factor-23, a phosphatonin that is released in response to phosphate overload, is independently associated with adverse outcomes in patients with and without chronic kidney disease. Direct effects of extracellular phosphate on vascular calcification or cardiovascular cell biology; adverse consequences of adaptive mechanisms activated to limit phosphate overload, such as left ventricular hypertrophy induced by fibroblast growth factor-23; or epidemiological associations of additional cardiovascular risk factors with chronic kidney disease may underlie these observations. We now review the pathophysiology of phosphate, its relationship with cardiovascular outcomes, the potential consequences for patient care related to dietary phosphate and phosphate binders, and the clinical relevance for patients without overt chronic kidney disease.

Authors+Show Affiliations

Nephrology Department, IIS-Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Madrid. egonzalezpa@senefro.orgNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

22425627

Citation

Gonzalez-Parra, Emilio, et al. "Phosphate: a Stealthier Killer Than Previously Thought?" Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology, vol. 21, no. 5, 2012, pp. 372-81.
Gonzalez-Parra E, Tuñón J, Egido J, et al. Phosphate: a stealthier killer than previously thought? Cardiovasc Pathol. 2012;21(5):372-81.
Gonzalez-Parra, E., Tuñón, J., Egido, J., & Ortiz, A. (2012). Phosphate: a stealthier killer than previously thought? Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology, 21(5), 372-81. https://doi.org/10.1016/j.carpath.2012.02.008
Gonzalez-Parra E, et al. Phosphate: a Stealthier Killer Than Previously Thought. Cardiovasc Pathol. 2012 Sep-Oct;21(5):372-81. PubMed PMID: 22425627.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Phosphate: a stealthier killer than previously thought? AU - Gonzalez-Parra,Emilio, AU - Tuñón,Jose, AU - Egido,Jesus, AU - Ortiz,Alberto, Y1 - 2012/03/16/ PY - 2011/11/19/received PY - 2012/02/20/revised PY - 2012/02/21/accepted PY - 2012/3/20/entrez PY - 2012/3/20/pubmed PY - 2013/2/6/medline SP - 372 EP - 81 JF - Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology JO - Cardiovasc Pathol VL - 21 IS - 5 N2 - The kidneys excrete excess dietary phosphate, and patients with chronic kidney disease may suffer from phosphate overload and hyperphosphatemia. In chronic kidney disease, hyperphosphatemia has emerged as a risk factor for vascular calcification, cardiovascular mortality, left ventricular hypertrophy, and progression of chronic kidney disease. Serum phosphate at the upper limits of normal has also been associated with adverse outcomes in patients with relatively preserved kidney function. Of note, hyperphosphatemia is not a sensitive indicator of phosphate overload. In this regard, increased circulating fibroblast growth factor-23, a phosphatonin that is released in response to phosphate overload, is independently associated with adverse outcomes in patients with and without chronic kidney disease. Direct effects of extracellular phosphate on vascular calcification or cardiovascular cell biology; adverse consequences of adaptive mechanisms activated to limit phosphate overload, such as left ventricular hypertrophy induced by fibroblast growth factor-23; or epidemiological associations of additional cardiovascular risk factors with chronic kidney disease may underlie these observations. We now review the pathophysiology of phosphate, its relationship with cardiovascular outcomes, the potential consequences for patient care related to dietary phosphate and phosphate binders, and the clinical relevance for patients without overt chronic kidney disease. SN - 1879-1336 UR - https://www.unboundmedicine.com/medline/citation/22425627/Phosphate:_a_stealthier_killer_than_previously_thought L2 - https://linkinghub.elsevier.com/retrieve/pii/S1054-8807(12)00028-2 DB - PRIME DP - Unbound Medicine ER -