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磷代谢与慢性肾脏病 被引量:10

Phosphorus metabolism and chronic kidney disease
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摘要 磷是生命体中重要的元素之一,在细胞代谢和组织结构上起关键作用。磷以磷酸根形式存在,在细胞内组成细胞膜和遗传物质,参与细胞能量代谢及信号传导;在细胞外是骨无机质和牙结构的主要成分之一,部分则存在于血液循环,即临床可检出的血磷。血磷是机体磷代谢状况的直接反应,肠道吸收、肾脏排泄、组织利用以及一系列调节因子共同作用决定血磷的平衡。在慢性肾衰竭患者中,由于肾功能减退及身体内分泌功能的变化,这种平衡被打破而呈现高磷状态,已证实高磷血症除与骨代谢相关外,与心血管事件的发生和死亡率关系也甚密切。本文将围绕正常磷代谢、慢性肾脏病患者磷代谢异常以及高磷血症治疗的新进展进行综述。 Phosphorus is an important element in the life of the body in cellular metabolism and structurc maintenance. Serum phosphorus is a direct reflection of phosphorus metabolism. The balanc, e of phosphorus is decided by intestine absorption,kidney excretion,and body usage as well as a series of regulatory factors. In patients with chronic renal failure,this balance is broken. Patients often show high phosphorus status due to renal dysfunction and pilysical changes in endocrine function. Hyperphosphatemia has been proved to be related with renal osteodystrophy, vascular calcification, cardiovascular events incidence and mortality. Sodium phosphate co-transporter is the common chamlel to determiue Ihe phosphate transport in small intestine and renal tubular epithelial cells. It is divided into three subtypes. The impact factors of sodium phosphate co-transporter include diet, PTH, VitD3, FGF-23 and so on. The current means of control of hyperphosphatemia primarily are dialysis, diet restrietion, and usage of phosphate binders. At the same time, the levels of serum calcium,PTH,and 1,25 (OH)2 D3 are required to control. The latest K/DIGO guidelines recommend that in C KD3 4,serum calcium and phosphorus levels should be eonttvlled within the normal range (caleimn: 8.5 - 10. 5 mg/dl, phosphorus 2. 5 -4. 5 mg/dl) ,while to CKD5 patients,serum phosphate should be as c, lose to normal range. All treatmem programs are determined according to the dynamic changes of oatients' conditions,rather than a oartictdar monitorinb data.
作者 王梦婧 陈靖
出处 《肾脏病与透析肾移植杂志》 CAS CSCD 北大核心 2011年第6期548-553,共6页 Chinese Journal of Nephrology,Dialysis & Transplantation
关键词 慢性肾脏病 磷代谢 高磷血症 chronic kidney disease phosphorus metabolism hyperphosphatemia
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参考文献34

  • 1Caverzasio J,Bonjour JP.Mechanism of rapid phosphate (Pi)transport adaptation to a single low Pi meal in rat renal brush border membrane.Pflugers Arch,1985,404(3):227-231.
  • 2Kestenbaum B.Phosphate metabolism in the setting of chronic kidney disease:significance and recommendations for treatment.Semin Dial,2007,20(4):286-294.
  • 3Portale AA,Halloran BP,Morris RC Jr.Dietary intake of phosphorus modulates the circadian rhythm in serum concentration of phosphorus.Implications for the renal production of 1,25-dihydroxyvitamin D.J Clin Invest,1987,80 (4):1147-1154.
  • 4Reshkin S J,Forgo J,Biber J,etal.Functional asymmetry of phosphate transport and its regulation in opossum kidney cells:phosphate "adaptation".Pflugers Arch,1991,419(3-4):256-262.
  • 5Murer H,Hernando N,Forster I,et al.Proximal tubular phosphate reabsorption:molecular mechanisms.Physiol Rev,2000,80 (4):1373-1409.
  • 6Murer H,Hernando N,Forster L,etal.Molecular mechanisms in proximal tubular and small intestinal phosphate reabsorption (plenary lecture).Mol Membr Biol,2001,18(1):3-11.
  • 7Ohkido I,Segawa H,Yanagida R,et al.Cloning,gene structure and dietary regulation of the type-Ⅱ c Na/Pi cotransporter in the mouse kidney.Pflugers Arch,2003,446(1):106-115.
  • 8Barac-Nieto M,Alfred M,Spitzer A.Phosphate depletion in opossum kidney cells:apical but not basolateral or transepithelial adaptions of Pi transport.Exp Nephrol,2001,9(4):258-264.
  • 9Bacic D,Lehir M,Biber J,et al.The renal Na +/phosphate cotransporter NaPi-Ⅱ a is internalized via the receptor-mediated endocytic route in response to parathyroid hormone.Kidney Int,2006,69(3):495-503.
  • 10付强,刘源.钙、磷与维生素D对动物骨代谢的影响研究进展[J].中国比较医学杂志,2006,16(8):502-505. 被引量:38

二级参考文献49

  • 1赵学智.血磷及钠磷协同转运子在慢性肾脏病继发性甲状旁腺机能亢进发生和发展中的作用[J].中华肾脏病杂志,2005,21(3):172-173. 被引量:7
  • 2Willian G.Importance of hyperphosphataemia in the cardio-renal axis.Nephrol Dial Transplant,2004,19(Suppl 1):I4-I8.
  • 3Murer H,Hernando N,Forster I,et al.Regulation of Na/Pi transporter in the proximal tubule.Annu Rev Physiol,2003,65(3):531-542.
  • 4Itoh N,Ornitz DM.Evolution of the FGF and FGFR gene families.Trends Genet,2004,20(11):563-569.
  • 5Yulia M,Ronen L.Calcineurin A (beta) is central to the expression of the renal type Ⅱ Na/Pi Co-transporter gene and to the regulation of renal phosphate transport.J Am Soc Nephrol,2004,15:2972-2980.
  • 6Francesco Locatelli,Jorge B.Management of disturbance of calcium and phosphate metabolism in chronic renal insufficiency,with emphasis on the control of hyperphosphataemia.Nephrol Dial Transplant,2002,17(5):723-731.
  • 7Roussanne MC,Lieberherr M.Human parathyroid cell proliferation in response to calcium,NPS R-467,calcitriol and phosphate.Eur J Clin Invest,2001,31(7):610-616.
  • 8Arcidiacono T.Renal osteodystrophy and vascular calcification.J Endocrinol Invest,2009,32(4 Suppl):21-26.
  • 9Mohlenkamp S,Moebus S,Schmermund A,et al.Assessment of the nature/history of coronary artery calcification and identification of its determinants.Rationale of the 2nd part of the Heinz Nixdorf Recall Study.Herz,2007,32(2):108-120.
  • 10Asci G,Ozkahya M,Duman S,et al.The link between cardiovascular and bone disease in hemodialysis patients.Nephrol Dial Transplant,2007,22(Suppl 6):214-217.

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