Chronic Kidney Disease-Mineral and Bone Disorders

Keith A. Hruska, Matthew J. Williams, Toshifumi Sugatani

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

3 Scopus citations


The disruption of a multiorgan systems biology produced by renal injury in early stages of kidney injury and disease was unrecognized until its elucidation during the investigation of the chronic kidney disease-mineral bone disorder (CKD-MBD). The disordered systems biology causes the CKD-MBD and contributes major components of increased cardiovascular risk for CKD patients. The outcome of the syndrome, in addition to previously recognized renal osteodystrophy (ROD), is increased cardiovascular mortality in CKD patients. The inception of the CKD-MBD was only recently realized to be with the early effects of kidney disease. Its pathophysiology involves circulating factors produced by renal repair and newly discovered hormones, such as fibroblast growth factor 23 (FGF-23) and cleaved klotho. Progressing from its inception, the disruption of the multiorgan system leads to the pathophysiology previously recognized as secondary hyperparathyroidism, hyperphosphatemia, calcitriol deficiency, and ROD that are now incorporated into the CKD-MBD syndrome, along with vascular disease (especially calcification) and cardiac disease (especially hypertrophy and heart failure). The new pathophysiology brings attention to extreme need for advances in treatment of the CKD-MBD, which is currently focused on the late components of the syndrome, and which have been shown in clinical trials not to affect the mortality associated with the syndrome.

Original languageEnglish
Title of host publicationChronic Renal Disease
Number of pages19
ISBN (Electronic)9780128158760
ISBN (Print)9780128158777
StatePublished - Jan 1 2019


  • Calcitriol
  • Cardiac hypertrophy
  • FGF-23
  • Klotho
  • Parathyroid hormone
  • Phosphorus
  • Renal osteodystrophy
  • Sclerostin
  • Vascular calcification
  • Wnt inhibitors


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