Effects of aging on chronic kidney disease mineral and bone disorder

Curr Opin Nephrol Hypertens. 2025 Jul 1;34(4):297-303. doi: 10.1097/MNH.0000000000001084. Epub 2025 May 2.

Abstract

Purpose of review: Aging and chronic kidney disease mineral and bone disorder (CKD-MBD) interact to worsen bone health, vascular calcification, and frailty in older patients. The altered FGF23-Klotho axis and disrupted mineral homeostasis emphasize the need for early interventions to mitigate fractures and cardiovascular complications in this vulnerable population. This review provides an updated overview of the current knowledge on CKD-MBD in older patients.

Recent findings: CKD-MBD exacerbates bone fragility and vascular calcification in older populations. Early vascular aging and cognitive decline are associated with increased mortality. Disruptions in calcium, phosphate, and vitamin D homeostasis accelerate bone loss and fracture risk, whereas secondary hyperparathyroidism worsens cardiovascular outcomes. Additionally, polypharmacy, sarcopenia, and cognitive impairment further intensified the clinical burden in aging CKD patients.

Summary: Aging potentially worsens CKD-MBD, vascular calcification, and cardiovascular disease in older patients. This growing field offers promising opportunities for further research to enhance understanding, improve bone health outcomes, and reduce fracture risk.

Keywords: aging; chronic kidney disease; mineral and bone disorder; vascular calcification.

Publication types

  • Review

MeSH terms

  • Age Factors
  • Aged
  • Aging* / metabolism
  • Bone Density
  • Cardiovascular Diseases
  • Chronic Kidney Disease-Mineral and Bone Disorder* / epidemiology
  • Chronic Kidney Disease-Mineral and Bone Disorder* / metabolism
  • Chronic Kidney Disease-Mineral and Bone Disorder* / physiopathology
  • Fibroblast Growth Factor-23
  • Fractures, Bone
  • Humans
  • Klotho Proteins
  • Renal Insufficiency, Chronic*
  • Risk Factors
  • Vascular Calcification* / epidemiology
  • Vascular Calcification* / metabolism
  • Vascular Calcification* / physiopathology

Substances

  • Fibroblast Growth Factor-23
  • FGF23 protein, human
  • Klotho Proteins
  • KL protein, human