Evaluation of Hypophosphatemia: Lessons From Patients With Genetic Disorders

被引：30

作者：

Bacchetta, Justine ^{[1
]}

Salusky, Isidro B. ^{[1
]}

机构：

[1] Univ Calif Los Angeles, David Geffen Sch Med, Div Pediat Nephrol, Los Angeles, CA 90095 USA

来源：

AMERICAN JOURNAL OF KIDNEY DISEASES | 2012年 / 59卷 / 01期

关键词：

Fibroblast growth factor 23 (FGF-23); hypophosphatemia; hypophosphatemic rickets; tumor-induced osteomalacia; GROWTH-FACTOR; 23; X-LINKED HYPOPHOSPHATEMIA; PHOSPHATE HOMEOSTASIS; KLOTHO; RICKETS; DISEASE; FGF23; REABSORPTION; MANAGEMENT; FACTOR-23;

D O I：

10.1053/j.ajkd.2011.08.035

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

100201 [内科学]; 100221 [泌尿外科学];

摘要：

Phosphate is a key component of several physiologic pathways, such as skeletal development, bone mineralization, membrane composition, nucleotide structure, maintenance of plasma pH, and cellular signaling. The kidneys have a key role in phosphate homeostasis, with 3 hormones having important roles in renal phosphate handling: parathyroid hormone, fibroblast growth factor 23 (FGF-23), and 1,25-dihydroxyvitamin D. Independent of the genetic diseases affecting the FGF-23 pathway (such as hypophosphatemic rickets), hypophosphatemia is a frequent condition encountered in daily practice, and untreated critical hypophosphatemia can induce hemolysis, rhabdomyolysis, respiratory failure, cardiac dysfunction, and neurologic impairment. Rapid correction thus is necessary to avoid severe complications. The aims of this teaching case are to summarize the causes and biological evaluation of hypophosphatemia and provide an overview of our current understanding of phosphate metabolism. Am J Kidney Dis. 59(1):152-159. (C) 2011 by the National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

引用

页码：152 / 159

页数：8

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