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成纤维细胞生长因子23与慢性肾脏病患者心血管疾病的关系 被引量:2

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摘要 慢性肾脏病(chronic kidney disease,CKD)作为当今世界所面临的严峻的公共卫生挑战[1],同样也是我们所需解决的棘手的问题。CKD存在病因复杂,病程长,预后影响因素多,个体差异大等特点,且受社会及个体经济条件影响大。CKD患者的首位死亡原因是心血管疾病,并使现今社会背负了巨大的医疗压力[2]。
作者 徐超 张蕾
出处 《新疆医学》 2017年第1期81-83,共3页 Xinjiang Medical Journal
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  • 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.

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