Pathophysiology of chronic kidney disease-mineral and bone disorder

被引:35
|
作者
Mac Way, Fabrice [1 ,2 ,3 ]
Lessard, Myriam [1 ,2 ,4 ]
Lafage-Proust, Marie-Helene [1 ,2 ]
机构
[1] Univ Lyon, INSERM, U1059, F-42023 St Etienne 2, France
[2] CHU St Etienne, F-42055 St Etienne 2, France
[3] Hotel Dieu Quebec, Nephrol, Quebec City, PQ G1R 2J6, Canada
[4] Hop Sacre Coeur Montreal, Ouest Montreal, PQ H4J 1C5, Canada
关键词
Parathyroid hormone; FGF23; Bone biopsy; Bone turnover; Osteomalacia; Secondary hyperparathyroidism; HYPERPLASTIC PARATHYROID-GLANDS; RENAL OSTEODYSTROPHY; CKD PATIENTS; SECONDARY HYPERPARATHYROIDISM; DEPRESSED EXPRESSION; DOWN-REGULATION; RECEPTOR; CALCIUM; FGF23; PTH;
D O I
10.1016/j.jbspin.2012.09.014
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Chronic kidney disease (CKD) alters the metabolism of several minerals, thereby inducing bone lesions and vessel-wall calcifications that can cause functional impairments and excess mortality. The histological bone abnormalities seen in CKD, known as renal osteodystrophy, consist of alterations in the bone turnover rate, which may be increased (osteitis fibrosa [OF]) or severely decreased (adynamic bone disease [AD]); abnormal mineralization (osteomalacia [OM]), and bone loss. Secondary hyperparathyroidism is related to early phosphate accumulation (responsible for FGF23 overproduction by bone tissue), decreased calcitriol production by the kidneys, and hypocalcemia. Secondary hyperparathyroidism is associated with OF. Other factors that affect bone include acidosis, chronic inflammation, nutritional deficiencies, and iatrogenic complications. (C) 2012 Published by Elsevier Masson SAS on behalf of the Societe Francaise de Rhumatologie.
引用
收藏
页码:544 / 549
页数:6
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