AI Article Synopsis

  • Derangements in mineral metabolism are a key aspect of chronic kidney disease-mineral and bone disorder (CKD-MBD), specifically in cats, affecting calcium homeostasis.
  • Recent research highlights fibroblast growth factor 23 (FGF23) and α-Klotho as important biomarkers for predicting CKD progression, although their impact on calcium balance and calcification is unclear.
  • The review emphasizes the need for more studies in cats to better understand the clinical effects of calcium disturbances in CKD-MBD and its consequences on mineralization in both human and feline patients.

Article Abstract

Derangements in mineral metabolism are one of the main entities in chronic kidney disease-mineral and bone disorder (CKD-MBD). This is the second of a two-part review of the physiology and pathophysiology of calcium homeostasis in feline CKD-MBD. While dysregulation in calcium homeostasis is known to contribute to the development of vascular calcification in CKD, evidence characterising the relationship between serum calcium concentration and nephrocalcinosis and nephrolithiasis is limited. Recently, fibroblast growth factor 23 (FGF23) and α-Klotho have gained increased research interest and been shown to be important biomarkers for the prediction of CKD progression in human patients. However, conflicting evidence exists on their role in calcium homeostasis and vascular and soft tissue calcification. This review details the pathophysiology of calcium disorders associated with CKD-MBD and its implications on vascular and soft tissue mineralisation in human and feline patients. Further prospective studies investigating the clinical consequences of calcium disturbances in cats with CKD are warranted and this may provide additional insight into the pathophysiology of feline CKD-MBD.

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Source
http://dx.doi.org/10.1016/j.tvjl.2021.105718DOI Listing

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