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Cited by 26Parathyroid Disorders and TreatmentsRenal function and acid-base balanceIron Metabolism and Disorders

Physiopathology of Phosphate Disorders

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Portales-Castillo, Ignacio, Rieg, Timo, Khalid, Sheikh B., Nigwekar, Sagar U., Neyra, Javier A.·2023·Advances in Kidney Disease and Health
DOI 10.1053/j.akdh.2022.12.011PMC PMC10565570
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Abstract

Intracellular phosphate is critical for cellular processes such as signaling, nucleic acid synthesis, and membrane function. Extracellular phosphate (Pi) is an important component of the skeleton. Normal levels of serum phosphate are maintained by the coordinated actions of 1,25-dihydroxyvitamin D3, parathyroid hormone and fibroblast growth factor-23, which intersect in the proximal tubule to control the reabsorption of phosphate via the sodium-phosphate cotransporters Npt2a and Npt2c. Furthermore, 1,25-dihydroxyvitamin D3 participates in the regulation of dietary phosphate absorption in the small intestine. Clinical manifestations associated with abnormal serum phosphate levels are common and occur as a result of genetic or acquired conditions affecting phosphate homeostasis. For example, chronic hypophosphatemia leads to osteomalacia in adults and rickets in children. Acute severe hypophosphatemia can affect multiple organs leading to rhabdomyolysis, respiratory dysfunction, and hemolysis. Patients with impaired kidney function, such as those with advanced CKD, have high prevalence of hyperphosphatemia, with approximately two-thirds of patients on chronic hemodialysis in the United States having serum phosphate levels above the recommended goal of 5.5 mg/dL, a cutoff associated with excess risk of cardiovascular complications. Furthermore, patients with advanced kidney disease and hyperphosphatemia (>6.5 mg/dL) have almost one-third excess risk of death than those with phosphate levels between 2.4 and 6.5 mg/dL. Given the complex mechanisms that regulate phosphate levels, the interventions to treat the various diseases associated with hypophosphatemia or hyperphosphatemia rely on the understanding of the underlying pathobiological mechanisms governing each patient condition.

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Authors
Portales-Castillo, I., Rieg, T., Khalid, S. B., Nigwekar, S. U., & Neyra, J. A.
Affiliations
  • University of South Florida (US)
  • Indus Hospital (PK)
  • Harvard University (US)
  • University of Alabama at Birmingham (US)
Corresponding author
Neyra, Javier A.
ORCID
Venue
Advances in Kidney Disease and Health
Publisher
Elsevier BV
Published
2023-03
Volume
30
Issue
2
Pages
177-188
ISSN
2949-8139 (ISSN-L)
DOI
10.1053/j.akdh.2022.12.011
PMC
PMC10565570
OpenAlex
W4322734150
Cited by
26
References
1
Citations by year
2026: 4 · 2025: 8 · 2024: 11 · 2023: 3
FWCI
1.09
Type
journal article
Language
en
Open access
Licence
Locations
  • Advances in Kidney Disease and Health (acceptedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute of Diabetes and Digestive and Kidney Diseases (1U01DK123818-01, IBX004968 A, P30 DK079337, R01DK110621, R01DK128208, U01DK12998)
  • National Institute of Biomedical Imaging and Bioengineering (1R01EB031813-01A1)
  • American Heart Association (19TPA34850116, DK076169, DK115255, SCR_001415)
  • Alnylam Pharmaceuticals
Topics
  • Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
  • Health Sciences › Medicine › Nephrology › Renal function and acid-base balance
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
Keywords
phosphate homeostasis, hypophosphatemia, hyperphosphatemia, serum phosphorus, 1,25-dihydroxyvitamin D3, parathyroid hormone, fibroblast growth factor 23, sodium-phosphate cotransporter, Npt2a, chronic kidney disease, hemodialysis, rickets, osteomalacia, rhabdomyolysis, cardiovascular risk
MeSH terms
Adult, Calcitriol, Child, Humans, Phosphates, Rickets, Hypophosphatemia, Hyperphosphatemia

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