期刊文献+

慢性肾脏病患者成纤维细胞生长因子23与肾功能及钙磷代谢的关系 被引量:22

Association of fibroblast growth factor 23 with calcium-phosphorus metabolism and renal function in patients with chronic kidney disease
原文传递
导出
摘要 目的探讨慢性肾脏病(CKD)患者随着肾功能的变化,其成纤维细胞生长因子23(FGF23)与钙磷代谢的关系。方法研究对象为2008年8月至2009年4月在上海交通大学附属第一人民医院肾内科住院的初诊CKD患者72例,按照肾小球滤过率(GFR)水平分为5组,另设健康对照组20例。抽取受试者静脉血并分离血清,以酶联免疫法检测FGF23、25(OH)VitD3、1,25(OH)2VitD3;全自动生化分析仪测量钙(Ca)、磷(P)、血肌酐(Scr)、尿素氮(BUN)、白蛋白(A1b)水平;免疫放射法测定全段甲状旁腺激素(iPTH)。结果CKD患者血清FGF23水平随GFR降低逐渐升高,在CKD4期和5期时,血FGF23、P、iPTH上升明显,1,25(OH),VitD3显著下降,与CKD1期差异有统计学意义(均P〈0.05)。CKD2~3期与CKD1期的FGF23、P、Ca、iPTH、活性维生素D水平差异均无统计学意义。血ca、25(OH)VitD3随着肾功能下降有降低趋势,但各期间差异均无统计学意义。Pearson相关分析显示,CKD1~5期logFGF23与P、logiFFH呈正相关(r=0.653,P〈0.01;r=0.800,P〈0.01),与GFR、1,25(OH)2VitD3呈负相关(r=-0.753,P〈0.01;r=-0.265,P〈0.05),与ca、25(OH)VitD3无相关。CKD1~3期logFGF23与logiPTH呈正相关(r=0.374,P〈0.05),而与Ca、P、25(OH)VitD3、1,25(OH)2VitD3、GFR均无相关。CKD4~5期logFGF23与P、logiPTH呈正相关(r=0.381,P〈0.05;r=0.515,P〈0.01),与GFR呈负相关(r=-0.654,P〈0.01),与ca、25(OH)VitD3、1,25(OH)2VitD3无相关。结论随着肾功能减退,血清FGF23、P、iPTH水平逐渐升高,活性维生素D水平逐渐下降,尤以CKD4~5期明显。在肾脏病早期阶段(CKD1~3期)血iPTH水平与FGF23有关。当GFR〈30ml/min时,肾功能状态、血磷、血iPTH均可影响血FGF23水平。 Objective To study the association of fibroblast growth factor 23 (FGF23) with calcium (Ca)-phosphorus (P) metabolism and renal function in patients with chronic kidney disease (CKD). Methods Serum samples of 20 healthy people and 72 CKD patients were collected. Patients were divided into five groups according to renal function. Levels of FGF23,25 (OH)VitD3, and 1,25(OH)2VitD3 were measured by ELISA. Intact parathyroid hormone (iPTH) was detected by immunoradiometric assay. Scr, BUN, calcium (C), phosphorus (P) and albumin were assessed by autobiochemistry machine. Results Levels of serum FGF23, P, iPTH increased gradually and 1,25(OH)2VitD3 decreased with the decline of renal function, especially in stages 4-5 of CKD, whose differences were significant. Pearson correlation analysis revealed, during CKD1-5 stages, logFGF23 was correlated with P, logiPTH, GFR, 1,25 (OH)2VitD3 (r=0.653, P〈0.01; r= 0.800, P〈0.01; r=-0.753, P〈0.01; r=-0.265, P〈0.05). During CKD1-3 stage, logFGF23 was positively correlated with logigFH (r=0.374, P〈0.05) and not correlated with P, GFR, 1,25(OH) 2VitD3. During CKD4-5 stages, logFGF23 was positively correlated with P, logiFFH (r=0.381, P〈 0.05; r= 0.515, P〈0.01) and negatively correlated with GFR (r=-0.654, P〈0.01). There were no correlations of logFGF23 with 25 (OH)VitD3 and Ca. Conclusions Levels of serum FGF23, P, iPTH increase and 1,25 (OH)2VitD3 decreases with the decline of renal function, especially during CKD4-5 stages. The level of FGF23 is associated with iPTH during CKD1-3 stage. When GFR〈30 ml/min, FGF23 level is affected by renal tunction, phosphorus and iPTH.
出处 《中华肾脏病杂志》 CAS CSCD 北大核心 2010年第2期81-85,共5页 Chinese Journal of Nephrology
关键词 肾疾病 慢性 成纤维细胞生长因子 甲状旁腺素 Kidney disease, chronic Fibroblast growth factor 23 Parathyroid hormone Phosphorus
  • 相关文献

参考文献20

  • 1Block GA, Klassen PS, Lazarus JM, et al. Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. J Am Soc Nephrol, 2004, 15: 2208-2218.
  • 2ADHR Consortium. Autosomal dominant hypophpsphataemic richets is associated with mutations in FGF23. Nat Genet, 2000, 26: 345-348.
  • 3Benet-PagesA, Orlik P, Strom TM, et al. An FGF23 missense mutation causes familial tumoral c.alcinosis with hyperphosphatemia. Hum Mol Genet, 2005, 14: 385-390.
  • 4Tenenhouse HS, Sabbagh Y. Novel phosphate-regulating genes in the pathogenesis of renal phosphate wasting disorders. Pflugers Arch, 2002, 444: 317-326.
  • 5Saito H, Kusano K, Kinosaki M, et al. Hmnan fibroblast growth factor-23 mutants suppress Na+-dependent phosphate co-transport activity and lalpha, 25-dihyd-roxyvitamin D3 production. J Biol Chem, 2003, 278: 2206-2211.
  • 6Larsson T, Marsell R, Schipani E, et al. Transgenic mice expressing fibroblast growth faetor-23 under the eontrol of the alphal (1) collagen promoter exhibit growth retardation, osteomalaeia and disturbed phosphate homeostasis. Endocrinology, 2004, 145: 3087-3094.
  • 7Razzaque MS, St-Arnaud R, Taguchi T, et al. FGF23, vitamin D and calcification:the unholy triad. Nephrol Dial Transplant, 2005, 20: 2032-2035.
  • 8Deluca S, Sitara D, Kang K, et al. Amelioration of the premature aging-like features of FGF23 knockout mice by genetieally restoring the systemic aclions of FCF23. J Pathol, 2008, 216: 345-355.
  • 9Gutierrez O, Isakova T, Rhee E, et al. Fibroblast growth fhctor-23 mitigates hyperphosphatemia but accentuates ealcitriol deficieney in chronic kidney disease. J Am Soc Nephrol, 2005, 16: 2205-2215.
  • 10Larsson T, Nisbeth U, I,junggren O, et al. Circulating eoncentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. Kidney Int, 2003, 64: 2272-2279.

同被引文献231

引证文献22

二级引证文献166

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部