Elevated FGF-23 in a patient with rhabdomyolysis-induced acute kidney injury

被引：30
|
作者：
Leaf, David E.
Wolf, Myles [2 ]
Stern, Leonard [1 ]
机构：
[1] Columbia Univ, Dept Med, Div Nephrol, New York, NY 10027 USA
[2] Univ Miami, Miller Sch Med, Dept Med, Div Nephrol & Hypertens, Miami, FL 33136 USA
来源：
NEPHROLOGY DIALYSIS TRANSPLANTATION | 2010年 / 25卷 / 04期
关键词：
ARF; hyperparathyroidism; hyperphosphataemia; vitamin D; FIBROBLAST GROWTH FACTOR-23; PARATHYROID-HORMONE; RENAL-FAILURE; SECONDARY HYPERPARATHYROIDISM; METABOLISM; RECEPTOR; FGF23;
D O I：
10.1093/ndt/gfp682
中图分类号：
R3 [基础医学]; R4 [临床医学];
学科分类号：
1001 ; 1002 ; 100602 ;
摘要：
Rhabdomyolysis-induced acute kidney injury (AKI) is characterized by hyperphosphataemia and hypocalcaemia. Despite appropriate secondary elevation of parathyroid hormone (PTH) in response to hypocalcaemia, rhabdo-myolysis and AKI are associated with acute deficiency of 1,25-dihydroxycholecalciferol (1,25(OH)(2)D-3), and yet, the mechanism responsible for such a deficiency remains unclear. Fibroblast growth factor 23 (FGF-23), a potent phosphaturic hormone that inhibits 25-hydroxyvitamin D-3-1 alpha-hydroxylase, could explain the deficiency of 1,25 (OH)(2)D-3 in this setting. Here, we document, for the first time, elevated levels of FGF-23 in a patient with rhabdomyolysis-induced AKI.
引用
收藏
页码：1335 / 1337
页数：3
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