期刊
SEMINARS IN NEPHROLOGY
卷 34, 期 2, 页码 151-163出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.semnephrol.2014.02.007
关键词
Calcium; hyperphosphatemia; vitamin D; uremic toxins; FGF23; klotho; PTH
资金
- Amgen
- Genzyme/Sanofi
- Shire
- Syskid
- Government of Spain
- Fresenius
- AbbVie
- Fresenius Medical Care
- Medice
- Mitsubishi
- Sanofi
- Vifor
Chronic kidney disease mineral and bone disorder (CKD-MBD) is characterized by bone abnormalities, vascular calcification, and an array of laboratory abnormalities. The latter classically include disturbances in the parathyroid hormone/vitamin D axis. More recently, fibroblast growth factor 23 (FGF23) and klotho also have been identified as important regulators of mineral metabolism. Klotho deficiency and high circulating F0F23 levels precede secondary hyperparathyroidism in CKD patients. Levels of FGF23 and parathyroid hormone increase along the progression of CKD to maintain mineral homeostasis and to overcome end-organ resistance. It is hard to define when the increase of both hormones becomes maladaptive. CKD-MBD is associated with adverse outcomes including cardiovascular disease and mortality. This review summarizes the complex pathophysiology of CKD-MBD and outlines which laboratory abnormalities represent biomarkers of disease severity, which laboratory abnormalities are predictors of cardiovascular disease, and which laboratory abnormalities should be considered (direct) uremic toxins exerting organ damage. This information may help to streamline current and future therapeutic efforts. Semin Nephrol 34:151-163 (C) 2014 Elsevier Inc. All rights reserved.
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