Elevation of circulating but not myocardial FGF23 in human acute decompensated heart failure
Elevation of circulating but not myocardial FGF23 in human acute decompensated heart failure
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DOI：
10.1093/ndt/gfv398
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发表时间：
2016-05-01
影响因子：
6.1
通讯作者：
Burnett, John C., Jr.
中科院分区：
文献类型：
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作者：
Andersen, Ingrid A.;Huntley, Brenda K.;Burnett, John C., Jr.
血浆成纤维细胞生长因子23（FGF 23）升高是慢性肾脏疾病的预后标志物。最近，有报道称FGF 23也是慢性充血性心力衰竭（HF）的预测因子。然而，迄今为止，急性失代偿性HF（ADHF）中的血浆水平尚未报道，并且HF中的心肌产生和FGF 23的分布不清楚。本研究检测了21例ADHF患者和19例对照者的血浆FGF 23、N末端B型利钠肽前体（NT-proBNP）和肾小球滤过率（eGFR）。在心力衰竭患者和正常对照组的左心室样本中测定心肌基因表达和FGF 23的分布，与对照组相比，ADHF患者的血浆FGF 23显著升高（1498 +/- 1238 vs 66 +/- 27 RU/mL，P < 0.0001）。FGF 23与eGFR、NT-proBNP、射血分数和年龄无相关性。eGFR > 60 mL/min/1.73 m2的ADHF受试者的FGF 23水平为1526 +/- 1601 RU/mL，而对照组为55 +/- 20 RU/mL（P = 0.007）。定量心肌FGF 23基因表达在HF患者和对照组之间相似。心肌FGF 23免疫染色在HF患者和对照组之间相似，在心肌细胞中分布均匀。心肌FGF 23基因表达在HF中与正常对照组相似，免疫组化显示HF和对照组中FGF 23的细胞分布相似，这表明心肌对HF中循环FGF 23的升高没有贡献。
Elevated plasma fibroblast growth factor 23 (FGF23) is a prognostic marker in chronic kidney disease. Recently, FGF23 was reported to also be a predictive factor in chronic congestive heart failure (HF). To date however, plasma levels in acute decompensated HF (ADHF) have not been reported and myocardial production and distribution of FGF23 in HF is poorly defined. We aimed to determine plasma levels and myocardial production of FGF23 in ADHF.Plasma FGF23, N-terminal pro B-type natriuretic peptide (NT-proBNP) and estimated glomerular filtration rate (eGFR) were assessed in 21 ADHF patients and 19 controls. Myocardial gene expression and distribution of FGF23 was determined on left ventricular samples from HF patients and normal controls.Plasma FGF23 was markedly higher in ADHF patients compared with controls (1498 +/- 1238 versus 66 +/- 27 RU/mL, P < 0.0001). There were no correlations between FGF23 and eGFR, NT-proBNP, ejection fraction or age. ADHF subjects with eGFR > 60 mL/min/1.73 m(2) had FGF23 levels of 1526 +/- 1601 RU/mL versus 55 +/- 20 RU/mL in controls (P = 0.007). Quantified myocardial FGF23 gene expression was similar between HF patients and controls. Myocardial FGF23 immunostaining was similar between HF patients and controls, with equal distribution throughout cardiomyocytes.Patients with ADHF had markedly elevated plasma FGF23 levels. Myocardial FGF23 gene expression was present in HF at a similar level as normal controls, and immunohistochemistry showed similar cellular distribution of FGF23 in HF and controls, suggesting that the myocardium does not contribute to the elevated circulating FGF23 in HF.