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Roles of Electrolytes: Calcium and Phosphate01:27

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Calcium and phosphate are essential electrolytes in the human body, with calcium being the most abundant mineral. Around 99% of the body's calcium is stored in the skeleton and teeth, forming a crystal lattice of mineral salts in combination with phosphates. Calcium plays crucial roles in various bodily functions such as blood clotting, neurotransmitter release, muscle tone maintenance, and nervous and muscle tissue excitability.
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The addition or removal of phosphate groups from proteins is the most common chemical modification that regulates cellular processes. These modifications can affect the structure, activity, stability, and localization of proteins within cells as well as their interactions with other proteins.
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Rab10 Phosphorylation Detection by LRRK2 Activity Using SDS-PAGE with a Phosphate-binding Tag
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Phosphate and Klotho.

Makoto Kuro-O1

  • 1Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.

Kidney International
|January 10, 2016
PubMed
Summary
This summary is machine-generated.

Decreased Klotho expression is an early sign of chronic kidney disease (CKD), driving CKD-mineral and bone disorder (CKD-MBD). Maintaining normal phosphate levels may mitigate these aging-related mineral and vascular issues.

Keywords:
FGF-23Klothobiomarkers of CKDhyperphosphatemiasecreted Klotho

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Area of Science:

  • Endocrinology
  • Nephrology
  • Aging Research

Background:

  • Klotho functions as an aging suppressor and co-receptor for Fibroblast Growth Factor 23 (FGF-23).
  • Klotho is crucial for regulating phosphate and calcium homeostasis within the bone-kidney-parathyroid axis.
  • Klotho deficiency in mice leads to premature aging and chronic kidney disease-mineral and bone disorder (CKD-MBD) phenotypes.

Purpose of the Study:

  • To establish decreased Klotho expression as the earliest biomarker of CKD.
  • To elucidate Klotho's role in initiating CKD-MBD pathophysiology.
  • To explore the therapeutic potential of maintaining normal phosphate levels in CKD patients with declining Klotho.

Main Methods:

  • Analysis of Klotho expression in different stages of chronic kidney disease (CKD).
  • Investigation of Klotho's FGF-23-dependent and independent functions.
  • Evaluation of phosphate-lowering interventions in preclinical models of Klotho deficiency.

Main Results:

  • Klotho expression declines progressively in humans from stage 1 CKD onwards.
  • Decreased Klotho causes FGF-23 resistance, leading to elevated FGF-23 and parathyroid hormone levels.
  • Secreted Klotho exhibits FGF-23-independent effects on phosphate and calcium regulation in renal tubules.

Conclusions:

  • Reduced Klotho expression is the earliest indicator of CKD and the primary driver of CKD-MBD.
  • CKD can be characterized as accelerated aging due to hyperphosphatemia and Klotho deficiency.
  • Therapeutic strategies targeting phosphate binders in CKD patients with low Klotho may prevent mineral and vascular complications.