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综述

继发性甲状旁腺功能亢进与肾移植相关并发症的研究进展

  • 刘晓怡 ,
  • 谢超 ,
  • 孔耀中
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  • 1广东佛山市第一人民医院肾内科

收稿日期: 2020-04-03

  修回日期: 2020-05-16

  网络出版日期: 2020-08-12

Recent advances in secondary hyperparathyroidism and the related complications after renal transplantation

  • LIU Xiao-Yi ,
  • XIE Chao ,
  • KONG Yao-Zhong
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  • 1Department of Nephrology, the First Foshan People's Hospital, Foshan 528000, China

Received date: 2020-04-03

  Revised date: 2020-05-16

  Online published: 2020-08-12

摘要

【摘要】继发性甲状旁腺功能亢进(secondary hyperparathyroidism,SHPT)是慢性肾脏病患者常见的并发症,肾移植成功后钙磷代谢等因素发生变化,导致患者出现甲状旁腺功能变化,但仍有部分患者合并甲状旁腺功能亢进(hyperparathyroidism,HPT)。近年来发现移植后HPT 可增加肾移植受者移植肾失功、骨代谢紊乱、心血管疾病、移植后糖尿病和死亡风险。本文将阐述SHPT与肾移植相关并发症的关系。

本文引用格式

刘晓怡 , 谢超 , 孔耀中 . 继发性甲状旁腺功能亢进与肾移植相关并发症的研究进展[J]. 中国血液净化, 2020 , 19(08) : 547 -549 . DOI: 10.3969/j.issn.1671-4091.2020.08.011

Abstract

【Abstract】 Secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease patients. Hyperparathyroidism may still occur in some patients after successful kidney transplantation due to the changes of calcium and phosphorus metabolism that lead to the abnormal functions of parathyroid gland. Recently, it is found that hyperparathyroidism after kidney transplantation increases the risks of loss functions of the graft, bone metabolic disorders, cardiovascular diseases, post-transplantation diabetes mellitus and death. In this paper, the relationship between SHPT and kidney transplantation related complications is discussed.

参考文献

[1]Ferrari P.Early kidney allograft loss-Is there scope for improvement?[J].Transpl Int, 2018, 31(8):864-866
[2]Evenepoel P.Recovery versus persistence of disordered mineral metabolism in kidney transplant recipients[J].Semin Nephrol, 2013, 33(2):191-203
[3]Almquist M, Isaksson E, Clyne N.The treatment of renal hyperparathyroidism[J].Endocr Relat Cancer, 2020, 27(1):R21-R34
[4]毛建萍, 张倩, 陈靖.慢性肾脏病患者甲状旁腺病变发生机制的研究新进展[J].中华肾脏病杂志, 2019, 35(8):630-634
[5]Bikbov B, Purcell C, Levey AS, et al.Global,regional,and national burden of chronic kidney disease,1990-2017: a systematic analysis for the Global Burden of Disease Study 2017[J].Lancet, 2020, 395,(10225):709-733
[6]Liabeuf S, McCullough K, Young EW, et al.International variation in the management of mineral bone disorder in patients with chronic kidney disease: Results from CKDopps[J].Bone, 2019, 129: 115058., 2019, 129:115058-
[7]Kong X, Zhang L, Zhang L, et al.Mineral and bone disorder in Chinese dialysis patients: a multicenter study[J].BMC Nephrology, 2012, 13:116-
[8]Wang J, Bieber BA, Hou FF, et al.Mineral and bone disorder and management in the China Dialysis Outcomes and Practice Patterns Study[J].Chin Med J (Engl), 2019, 132(23):2775-2782
[9]Martin M, Valls J, Betriu A, et al.Association of serum phosphorus with subclinical atherosclerosis in chronic kidney diseaseSex makes a difference[J].Atherosclerosis, 2015, 241(1):264-270
[10]Yamamoto D, Suzuki S, Ishii H, et al.Predictors of abdominal aortic calcification progression in patients with chronic kidney disease without hemodialysis[J].Atherosclerosis, 2016, 253:15-21
[11]Block GA, Klassen PS, Lazarus JM, et al.Mineral metabolism, mortality, and morbidity in maintenance hemodialysis[J]. J Am Soc Nephrol, 2004, 15(8):, 2004, 15(8):2208-2218
[12]韦星, 蔡明, 金海龙等.肾移植术后继发性甲状旁腺功能亢进的临床分析[J].中华移植杂志电子版, 2018, 12(2):60-64
[13]Lou I, Foley D, Odorico SK, et al.How Well Does Renal Transplantation Cure Hyperparathyroidism?[J].Ann Surg, 2015, 262(4):653-659
[14]李宁, 王明君, 郭文萍等.肾移植前后矿物质和骨代谢变化的临床研究[J].中华器官移植杂志, 2016, 37(11):647-652
[15]Alagoz S, Trabulus S.Long-Term Evaluation of Mineral Metabolism After Kidney Transplantation[J].Transplantation proceedings, 2019, 51(7):2330-2333
[16]Taniguchi M, Tokumoto M, Matsuo D, et al.Persistent hyperparathyroidism in renal allograft recipients: vitamin D receptor,calcium-sensing receptor,and apoptosis[J].Kidney Int, 2006, 70(2):363-370
[17]Bravo J, Esteban RJ, Medina A, et al.Successful kidney transplantation reduces hyperplastic parathyroid gland[J].Transplantation proceedings, 2007, 39(1):125-131
[18]Pihlstr?m H, Dahle DO, Mj?en G, et al.Increased risk of all-cause mortality and renal graft loss in stable renal transplant recipients with hyperparathyroidism[J].Transplantation, 2015, 99(2):351-359
[19]Prakobsuk S, Sirilak S, Vipattawat K, et al.Hyperparathyroidism and increased fractional excretion of phosphate predict allograft loss in long-term kidney transplant recipients[J].Clin Exp Nephrol, 2017, 21(5):926-931
[20]eltik A, ?en S, Y?lmaz M, et al.The effect of hypercalcemia on allograft calcification after kidney transplantation[J].Int Urol Nephrol, 2016, 48(11):1919-1925
[21]李宁.肾移植术后矿物质和骨异常[J].器官移植, 2019, 10(5):559-569
[22]Moiz A, Javed T, Garces J, et al.Posttransplant nephrocalcinosis is associated with poor renal allograft function: a single-center experience[J].Ochsner J, 2015, 15(1):25-29
[23]Hiemstra TF, Brown AJD, Chaudhry AN, et al.Association of calcium,phosphate and parathyroid hormone with renal allograft function: a retrospective cohort study[J].Am J Nephrol, 2013, 37(4):339-345
[24]Garcia-Montemayor V, Sánchez-Agesta M, Agüera ML, et al.Influence of Pre-renal Transplant Secondary Hyperparathyroidism on Later Evolution After Transplantation[J].Transplantation proceedings, 2019, 51(2):344-349
[25]Amin T, Coates PT, Barbara J, et al.Prevalence of hypercalcaemia in a renal transplant population: a single centre study [J]. Int J Nephrol, 2016, 2016: 7126290.[J]. Int J Nephrol, 2016, 2016:7126290-
[26]Taweesedt PT, Disthabanchong S.Mineral and bone disorder after kidney transplantation[J].World J Transplant, 2015, 5(4):231-242
[27]Altman AM, Sprague SM.Mineral and bone disease in kidney transplant recipients[J].Curr Osteoporos Rep, 2018, 16(6):703-711
[28]Park WY, Han S, Choi BS, et al.Progression of Osteoporosis After Kidney Transplantation in Patients With End-Stage Renal Disease[J].Transplantation proceedings, 2017, 49(5):1033-1037
[29]Perrin P, Kiener C, Javier R-M, et al.Recent Changes in Chronic Kidney Disease-Mineral and Bone Disorders and Associated Fractures After Kidney Transplantation[J].Transplantation, 2017, 101(8):1897-1905
[30]Perrin P, Caillard S, Javier RM, et al.Persistent hyperparathyroidism is a major risk factor for fractures in the five years after kidney transplantation[J].Am J Transplant, 2013, 13(10):2653-2663
[31]Ferro CJ, Arnold J, Bagnall D, et al.Fracture risk and mortality post-kidney transplantation[J].Clin Transplant, 2015, 29(11):1004-1012
[32]Cruzado JM, Moreno P, Torregrosa JV, et al.A Randomized Study Comparing Parathyroidectomy with Cinacalcet for Treating Hypercalcemia in Kidney Allograft Recipients with Hyperparathyroidism[J].J Am Soc Nephrol, 2016, 27(8):2487-2494
[33]Vaidya A, Brown JM, Williams JS.The renin-angiotensin-aldosterone system and calcium-regulatory hormones[J].J Hum Hypertens, 2015, 29(9):515-521
[34]Bleskestad IH, Bergrem H, Leivestad T, et al.Parathyroid hormone and clinical outcome in kidney transplant patients with optimal transplant function[J].Clin Transplant, 2014, 28(4):479-486
[35]Ivarsson KM, Akaberi S, Isaksson E, et al.Cardiovascular and Cerebrovascular Events After Parathyroidectomy in Patients on Renal Replacement Therapy[J].World J Surg, 2019, 43(8):1981-1988
[36]Cheng ZY, Ye T, Ling QY, et al.Parathyroid hormone promotes osteoblastic differentiation of endothelial cells via the extracellular signalregulated protein kinase 12 and nuclear factorκB signaling pathways[J].Exp Ther Med, 2017, 15(2):1754-1760
[37]Carrillo-López N, Panizo S, Alonso-Montes C, et al.High-serum phosphate and parathyroid hormone distinctly regulate bone loss and vascular calcification in experimental chronic kidney disease[J].Nephrol Dial Transplant, 2019, 34(6):934-941
[38]Baia LC, Humalda JK, Vervloet MG, et al.Fibroblast growth factor 23 and cardiovascular mortality after kidney transplantation[J].Clin J Am Soc Nephrol, 2013, 8(11):1968-1978
[39]Di Lullo L, Gorini A, Bellasi A, et al.Fibroblast growth factor 23 and parathyroid hormone predict extent of aortic valve calcifications in patients with mild to moderate chronic kidney disease[J].Clin Kidney J, 2015, 8(6):732-736
[40]Rodelo-Haad C, Santamaria R, Mu?oz-Casta?eda JR, et al.FGF23,Biomarker or Target?[J].Toxins (Basel), 2019, 11(3):175-
[41]Blau JE, Collins MT.The PTH-Vitamin D-FGF23 axis[J].Reviews in Endocrine and Metabolic Disorders, 2015, 16(2):165-174
[42]Lee SA, Lee MJ, Ryu GW, et al.Low serum intact parathyroid hormone level is an independent risk factor for overall mortality and major adverse cardiac and cerebrovascular events in incident dialysis patients[J].Osteoporos Int, 2016, 27(9):2717-2726
[43]Isaksson E, Almquist M, Seeberger A, et al.Is low pre-transplant parathyroid hormone a risk marker for cardiovascular disease in long-term follow-up of renal transplant recipients?[J].Clin Exp Nephrol, 2018, 22(5):1188-1197
[44]Rojas E, Carlini RG, Clesca P, et al.The pathogenesis of osteodystrophy after renal transplantation as detected by early alterations in bone remodeling[J].Kidney Int, 2003, 63(5):1915-1923
[45]Cannata-Andia JB, Roman-Garcia P, Hruska K.The connections between vascular calcification and bone health[J].Nephrol Dial Transplant, 2011, 26(11):3429-3436
[46]Burroughs TE, Swindle J, Takemoto S, et al.Diabetic complications associated with new-onset diabetes mellitus in renal transplant recipients[J].Transplantation, 2007, 83(8):1027-1034
[47]Sinangil A, Celik V, Barlas S, et al.The incidence of new onset diabetes after transplantation and related factors: Single center experience[J].Nefrologia, 2017, 37(2):181-188
[48]Ivarsson KM, Clyne N, Almquist M, et al.Hyperparathyroidism and new onset diabetes after renal transplantation[J].Transplantation proceedings, 2014, 46(1):145-150
[49]Procopio M, Borretta G.Derangement of glucose metabolism in hyperparathyroidism[J].J Endocrinol Invest, 2003, 26(11):1136-1142
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