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Chronic Kidney Disease (CKD) arises when the kidneys progressively lose their ability to function, ultimately leading to end-stage renal disease. At this advanced stage, the kidneys can no longer filter waste or maintain essential body functions, requiring renal replacement therapy (RRT) through dialysis or a kidney transplant for survival.Early-stage chronic kidney disease and detection challengesIn CKD's early stages, symptoms often remain absent because healthy nephrons compensate for...
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Current Controversies on Adequate Circulating Vitamin D Levels in CKD.

Adriana S Dusso1, Daniela J Porta1, Carlos Bernal-Mizrachi1,2

  • 1Division of Endocrinology, Metabolism and Lipid Research, Washington University School of Medicine, St. Louis, MO 63110, USA.

International Journal of Molecular Sciences
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PubMed
Summary

Management of secondary hyperparathyroidism in chronic kidney disease has shifted focus to the vitamin D endocrine system, FGF23-Klotho axis, and nutritional vitamin D status. These advancements reveal complex pathophysiology beyond PTH control, necessitating nuanced therapeutic strategies.

Keywords:
FGF23calcidiolcalcitriolcardiovascular damageklothorenal damagevitamin D

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Area of Science:

  • Endocrinology
  • Nephrology
  • Mineral Metabolism

Background:

  • Secondary hyperparathyroidism (SHPT) management in chronic kidney disease (CKD) has evolved significantly over 50 years.
  • Understanding of the vitamin D endocrine system's role in CKD progression has been reshaped by key discoveries.
  • Three critical paradigm shifts have altered the approach to SHPT in CKD.

Purpose of the Study:

  • To synthesize pathophysiological insights and clinical evidence underlying major shifts in SHPT management in CKD.
  • To review the evolution from calcitriol replacement to selective vitamin D receptor activators (VDRAs).
  • To discuss the impact of nutritional vitamin D deficiency and the FGF23-Klotho axis on CKD pathophysiology and treatment.

Main Methods:

  • Review of key pathophysiological insights in SHPT and CKD.
  • Synthesis of clinical evidence related to vitamin D therapy and the FGF23-Klotho axis.
  • Analysis of the therapeutic dilemmas posed by current treatment strategies.

Main Results:

  • Selective vitamin D receptor activators (VDRAs) offer survival benefits beyond mineral metabolism.
  • Nutritional vitamin D deficiency is prevalent in CKD, posing mortality risks, but optimal management is controversial.
  • The FGF23-Klotho axis presents a therapeutic dilemma: VDRAs increase FGF23, while calcimimetics do not improve Klotho.

Conclusions:

  • SHPT management in CKD is complex, involving intricate interactions beyond PTH control.
  • Nuanced therapeutic strategies are needed to balance FGF23 burden and Klotho preservation.
  • Overcoming diagnostic limitations in monitoring the FGF23-Klotho axis is crucial for personalized therapy and improved CKD outcomes.