Disorders of Mineral and Bone Metabolism in Chronic Kidney Disease

Keith A. Hruska, Michael E. Seifert, Kameswaran Surendran

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

Abstract

The disruption of 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 to major components of increased cardiovascular risk for CKD patients. The result, in addition to the previously recognized renal osteodystrophy, is increased cardiovascular mortality in CKD. The inception of the CKD-MBD was only recently realized to begin with the early effects of kidney disease, and its pathophysiology involves circulating factors produced by renal repair and newly discovered hormones, such as FGF23 and cut klotho. Progressing from its inception, the disruption of the multiorgan system leads to the pathophysiology previously recognized as secondary hyperparathyroidism, hyperphosphatemia, calcitriol deficiency, and renal osteodystrophy that are now incorporated into the CKD-MBD syndrome.

Original languageEnglish
Title of host publicationChronic Renal Disease
PublisherElsevier Inc.
Pages320-331
Number of pages12
ISBN (Electronic)9780124116160
ISBN (Print)9780124116023
DOIs
StatePublished - 2015

Keywords

  • Bone
  • Calcification
  • Calcitriol
  • Calcium
  • Fibroblast growth factor 23
  • Hyperparathyroidism
  • Klotho
  • Mineral
  • Osteodystrophy

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