Tags

Type your tag names separated by a space and hit enter

Prevention and control of phosphate retention/hyperphosphatemia in CKD-MBD: what is normal, when to start, and how to treat?
Clin J Am Soc Nephrol 2011; 6(2):440-6CJ

Abstract

Phosphate retention and, later, hyperphosphatemia are key contributors to chronic kidney disease (CKD)-mineral and bone disorder (MBD). Phosphate homeostatic mechanisms maintain normal phosphorus levels until late-stage CKD, because of early increases in parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF-23). Increased serum phosphorus, and these other mineral abnormalities, individually and collectively contribute to bone disease, vascular calcification, and cardiovascular disease. Earlier phosphate control may, therefore, help reduce the early clinical consequences of CKD-MBD, and help control hyperphosphatemia and secondary hyperparathyroidism in late-stage CKD. Indeed, it is now widely accepted that achieving normal phosphorus levels is associated with distinct clinical benefits. This therapeutic goal is achievable in CKD stages 3 to 5 but more difficult in dialysis patients. Currently, phosphate control is only initiated when hyperphosphatemia occurs, but a potentially beneficial and simple approach may be to intervene earlier, for example, when tubular phosphate reabsorption is substantially diminished. Early CKD-MBD management includes dietary phosphate restriction, phosphate binder therapy, and vitamin D supplementation. Directly treating phosphorus may be the most beneficial approach because this can reduce serum phosphorus, PTH, and FGF-23. This involves dietary measures, but these are not always sufficient, and it can be more effective to also consider phosphate binder use. Vitamin D sterols can improve vitamin D deficiency and PTH levels but may worsen phosphate retention and increase FGF-23 levels, and thus, may also require concomitant phosphate binder therapy. This article discusses when and how to optimize phosphate control to provide the best clinical outcomes in CKD-MBD patients.

Authors+Show Affiliations

Division of Nephrology, St. Louis University School of Medicine, 3635 Vista Avenue, St. Louis, MO 63110, USA. martinkj@slu.eduNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

21292848

Citation

Martin, Kevin J., and Esther A. González. "Prevention and Control of Phosphate Retention/hyperphosphatemia in CKD-MBD: what Is Normal, when to Start, and How to Treat?" Clinical Journal of the American Society of Nephrology : CJASN, vol. 6, no. 2, 2011, pp. 440-6.
Martin KJ, González EA. Prevention and control of phosphate retention/hyperphosphatemia in CKD-MBD: what is normal, when to start, and how to treat? Clin J Am Soc Nephrol. 2011;6(2):440-6.
Martin, K. J., & González, E. A. (2011). Prevention and control of phosphate retention/hyperphosphatemia in CKD-MBD: what is normal, when to start, and how to treat? Clinical Journal of the American Society of Nephrology : CJASN, 6(2), pp. 440-6. doi:10.2215/CJN.05130610.
Martin KJ, González EA. Prevention and Control of Phosphate Retention/hyperphosphatemia in CKD-MBD: what Is Normal, when to Start, and How to Treat. Clin J Am Soc Nephrol. 2011;6(2):440-6. PubMed PMID: 21292848.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prevention and control of phosphate retention/hyperphosphatemia in CKD-MBD: what is normal, when to start, and how to treat? AU - Martin,Kevin J, AU - González,Esther A, Y1 - 2011/02/03/ PY - 2011/2/5/entrez PY - 2011/2/5/pubmed PY - 2011/6/8/medline SP - 440 EP - 6 JF - Clinical journal of the American Society of Nephrology : CJASN JO - Clin J Am Soc Nephrol VL - 6 IS - 2 N2 - Phosphate retention and, later, hyperphosphatemia are key contributors to chronic kidney disease (CKD)-mineral and bone disorder (MBD). Phosphate homeostatic mechanisms maintain normal phosphorus levels until late-stage CKD, because of early increases in parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF-23). Increased serum phosphorus, and these other mineral abnormalities, individually and collectively contribute to bone disease, vascular calcification, and cardiovascular disease. Earlier phosphate control may, therefore, help reduce the early clinical consequences of CKD-MBD, and help control hyperphosphatemia and secondary hyperparathyroidism in late-stage CKD. Indeed, it is now widely accepted that achieving normal phosphorus levels is associated with distinct clinical benefits. This therapeutic goal is achievable in CKD stages 3 to 5 but more difficult in dialysis patients. Currently, phosphate control is only initiated when hyperphosphatemia occurs, but a potentially beneficial and simple approach may be to intervene earlier, for example, when tubular phosphate reabsorption is substantially diminished. Early CKD-MBD management includes dietary phosphate restriction, phosphate binder therapy, and vitamin D supplementation. Directly treating phosphorus may be the most beneficial approach because this can reduce serum phosphorus, PTH, and FGF-23. This involves dietary measures, but these are not always sufficient, and it can be more effective to also consider phosphate binder use. Vitamin D sterols can improve vitamin D deficiency and PTH levels but may worsen phosphate retention and increase FGF-23 levels, and thus, may also require concomitant phosphate binder therapy. This article discusses when and how to optimize phosphate control to provide the best clinical outcomes in CKD-MBD patients. SN - 1555-905X UR - https://www.unboundmedicine.com/medline/citation/21292848/full_citation L2 - http://cjasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=21292848 DB - PRIME DP - Unbound Medicine ER -