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慢性肾脏病患者甲状旁腺增生机制研究新进展 被引量：9

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摘要 继发性甲状旁腺功能亢进（secondary hyper-parathyroidismSHPT）是慢性肾脏病（chronic kid-neydisease,CKD）患者钙磷代谢紊乱和维生素D作用减退进行性加重的适应性反应,其特征是甲状旁腺增牛和甲状旁腺素（parathyroid hormone PTH）过度合成和分泌，进而导致骨过度重吸收，软组织和血管钙化，
作者 张倩 陈靖
机构地区 复旦大学附属华山医院肾病科
出处 《中国血液净化》 2008年第11期622-625,共4页 Chinese Journal of Blood Purification
关键词 继发性甲状旁腺功能亢进 慢性肾脏病 增生机制 病患 钙磷代谢紊乱 适应性反应 进行性加重 甲状旁腺素
分类号 R692.5 [医药卫生—泌尿科学] R692 [医药卫生—泌尿科学]
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参考文献35

  • 1Drueke TB. Cell biology of parathyroid gland hyperplasia in chronic renal failuref[J].J Am Soc Nephrol, 2000, 11:1141-1152.
  • 2Brown EM, MacLeod RJ. Extracellular calcium sensing and extracellular calcium signaling[J]. Physiol Rev ,2001, 81:239-297.
  • 3Henley C, Davis J, Miller G, et al. Calcium gluconate increases iCa, attenuates pPTH and parathyroid (PT) hyperplasia in uremic rats without causing calcification:Ab stract 162 presented at National Kidney Foundation Spring Clinical Meeting, 19-23 April 2006: Chicago.
  • 4Roussanne MC, Lieberherr M, Souberbielle JC, et al. Human parathyroid cell proliferation in response to calcium, NPS R-467, calcitriol and phosphate[J]. Eur J Clin Invest, 2001, 31:610-616.
  • 5D'Souza-Li L, Yang B, Canaff L, et al. Identification and functional characterization of novel calcium sensing re ceptor mutations in familial hypocalciuric hypcrcalcemia and autosomal dominant hypocalcemia[J]. J Clin Endocrinol Metab. 2002. 87:1309?318.
  • 6Gogusev J, Duchambon P, Hory B, et al. Depressed expression of calcium receptor in parathyroid gland tissue of pa tients with hyperparathyroidism[J]. Kidney Int, 1997, 51: 328-336.
  • 7Nemeth EF, Heaton Wll, Miller M, et al. Pharmacoldynamics of the type Ⅱ calcimimetic compound cinacalcet HCI[J].J Pharmacol Exp Ther, 2004, 308:627- 635.
  • 8Goodman WG, Frazao JM, Goodkin DA, et al. A calcimimetic agent lowers plasma parathyroid hormone levels in patients with secondary hyperparathyroidism[J]. Kidney Int,2000, 58:436-445.
  • 9Levi R, Ben Dov IZ, Lavi-Moshayoff V, et al. Increased parathyroid hormone gene expression in seeondacy hyperparathyroidism of experimental uremia is reversed by fication of the trans acting factoc AUF1[J].J Am Soc Nephrol ,2006, 17:107-112.
  • 10Colloton M,Shatzen E,Miller G,et al.Cinacalcet HCl attenuates parathyroid hyperplasia in a rat model of secondary hyperparathyroidism[J].Kidney Int,2005, 67:467-476.

二级参考文献15

  • 1杜学海.尿毒症继发性甲状旁腺功能亢进治疗进展:钙敏感受体激动剂[J].中国血液净化,2005,4(4):175-177. 被引量：4
  • 2Kenneth B, Jonsson. The role of fibroblast growth factor 23 in renal disease[J]. Nephrol Dial Transplant, 2005, 20: 479-482.
  • 3Gutierrez O, Isakova T, Rhee E, et al. Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency Jn chronic kidney disease[J]. J Am Soc Nephrol, 2005,16:2205-2215.
  • 4Collins MT, Lindsay JR, Jain A, et al. Fibroblast growth factor-23 is regulated by lalpha, 25-dihydroxyvitamin D [J]. J Bone Miner Res, 2005,20:1944-1950.
  • 5Fukagawa M, Kazama JJ. FGF23: its role in renal bone disease[J]. Pediatr Nephrol, 2006,21:1802-1806.
  • 6Westerberg PA, Linde T, Wikstrom B, et al. Regulation of fibroblast growth factor-23 in chronic kidney disease [J]. Nephrol Dial Transplant, 2007,22:3202-3207.
  • 7Tortes PU, Friedlander G, MC de Vernejoul et al. Bone mass does not correlate with the serum fibroblast growth factor 23 in hemodialysis patients[J].Kidney Int, 2008, 73:102- 107.
  • 8Nishi H, Nii-Kono T, Nakanishi S, et al. Intravenous calcitriol therapy increases serum concentrations of fibroblast growth factor-23 in dialysis patients with secondary hyperparathyroidism[J]. Nephron Clin Praet, 2005, 101: c94-c99.
  • 9陈旻译.血清磷水平的评价.王海燕,王梅主译,慢性肾脏病及透析的临床实践指南Ⅱ[M].第一版.北京,人民卫生出版社,2005,347-349.
  • 10Kazama JJ, Sato F, Omori K, et al. Pretreatment serum FGF- 23 levels predict the efficacy of calcitriol therapy in dialysis patients[J]. Kidney Int, 2005, 67: 1120-1125.

同被引文献96

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二级引证文献61

中国血液净化
2008年 第11期

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