[1]陈 丹,蒋霄翔,周丽佳,等.肾素-血管紧张素-醛固酮系统对维持性血透患者骨转换的影响[J].医学信息,2025,38(18):74-77.[doi:10.3969/j.issn.1006-1959.2025.18.016]
 CHEN Dan,JIANG Xiaoxiang,ZHOU Lijia,et al.Effect of Renin-angiotensin-aldosterone System on Bone Turnoverin Maintenance Hemodialysis Patients[J].Journal of Medical Information,2025,38(18):74-77.[doi:10.3969/j.issn.1006-1959.2025.18.016]
点击复制

肾素-血管紧张素-醛固酮系统对维持性血透患者骨转换的影响()

医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
38卷
期数:
2025年18期
页码:
74-77
栏目:
论著
出版日期:
2025-09-15

文章信息/Info

Title:
Effect of Renin-angiotensin-aldosterone System on Bone Turnoverin Maintenance Hemodialysis Patients
文章编号:
1006-1959(2025)18-0074-04
作者:
陈 丹蒋霄翔周丽佳胡跃一
温州医科大学附属慈溪医院肾内科,浙江 慈溪 315300
Author(s):
CHEN Dan JIANG Xiaoxiang ZHOU Lijia HU Yueyi
Department of Nephrology, Cixi Hospital Affiliated to Wenzhou Medical University, Cixi 315300, Zhejiang, China
关键词:
维持性血透肾素-血管紧张素-醛固酮系统骨转换
Keywords:
Maintenance hemodialysis Renin-angiotensin-aldosterone system Bone turnover
分类号:
R692.5
DOI:
10.3969/j.issn.1006-1959.2025.18.016
文献标志码:
A
摘要:
目的 观察肾素-血管紧张素-醛固酮系统(RAAS)对维持性血透患者骨转换的影响。方法 选取2020年11月-2022年5月慈溪市人民医院就诊的72例维持性血透患者。依据血管紧张素Ⅱ水平,将患者分为血管紧张素Ⅱ正常组(血管紧张素Ⅱ<90 pg/ml,41例)和血管紧张素Ⅱ升高组(血管紧张素Ⅱ≥90 pg/ml,31例)。采用Pearson相关性分析和多元线性回归分析探究维持性血透患者骨转换的影响因素。结果 血管紧张素Ⅱ升高组甲状旁腺激素、β-CTX、ALP水平均高于血管紧张素Ⅱ正常组,差异有统计学意义(P<0.01)。Pearson相关分析显示,β-CTX与血管紧张素Ⅱ、醛固酮、甲状旁腺激素呈正相关(P<0.05),ALP与血管紧张素Ⅱ、醛固酮、甲状旁腺激素呈正相关(P<0.01),甲状旁腺激素与血管紧张素Ⅱ、醛固酮呈正相关(P<0.05)。线性回归分析结果显示,甲状旁腺激素升高与Ⅰ型胶原交联C末端肽独立相关(β=0.672,P=0.000),血管紧张素Ⅱ升高与碱性磷酸酶独立相关(β=0.281,P=0.014),甲状旁腺激素升高与碱性磷酸酶独立相关(β=0.559,P=0.000)。结论 维持性血透患者骨转换标志物β-CTX、ALP均显著增高,且与血管紧张素Ⅱ、醛固酮呈正相关,RAAS与慢性肾衰竭维持性血透患者的异常骨转换有关,可能参与慢性肾脏病-矿物质和骨代谢紊乱(CKD-MBD)的发病与进展过程。
Abstract:
Objective To observe the effect of renin-angiotensin-aldosterone system (RAAS) on bone turnover in maintenance hemodialysis patients. Methods A total of 72 patients with maintenance hemodialysis who were treated in Cixi People’s Hospital from November 2020 to May 2022 were selected. According to the level of angiotensin II, the patients were divided into normal angiotensin Ⅱ group (angiotensin Ⅱ<90 pg/ml, 41 patients) and elevated angiotensin Ⅱgroup (angiotensin Ⅱ≥90 pg/ml, 31 patients). Pearson correlation analysis and multiple linear regression analysis were used to explore the influencing factors of bone turnover in maintenance hemodialysis patients. Results The levels of parathyroid hormone, β-CTX and ALP in the elevated angiotensin Ⅱ group were higher than those in the normal angiotensin Ⅱ group, and the differences were statistically significant (P<0.01). Pearson correlation analysis showed that β-CTX was positively correlated with angiotensin Ⅱ, aldosterone and parathyroid hormone (P<0.05), ALP was positively correlated with angiotensin Ⅱ, aldosterone and parathyroid hormone (P<0.01), and parathyroid hormone was positively correlated with angiotensin Ⅱ and aldosterone (P<0.05). Linear regression analysis showed that elevated parathyroid hormone was independently associated with type I collagen cross-linked C-terminal peptide (β=0.672, P=0.000), elevated angiotensin Ⅱ was independently associated with alkaline phosphatase (β=0.281, P=0.014), and elevated parathyroid hormone was independently associated with alkaline phosphatase (β=0.559, P=0.000). Conclusion The bone turnover markers β-CTX and ALP in maintenance hemodialysis patients are significantly increased, and are positively correlated with angiotensin Ⅱ and aldosterone. RAAS is related to abnormal bone turnover in maintenance hemodialysis patients with chronic renal failure, and may be involved in the pathogenesis and progression of chronic kidney disease-mineral and bone metabolism disorder (CKD-MBD).

参考文献/References:

[1]Jia XY,Wei K,Chen J,et al.Association of plasma neutrophil gelatinase-associated lipocalin with parameters of CKD-MBD in maintenance hemodialysis patients[J].J Bone Miner Metab,2021,39(6):1058-1065.[2]漆映辉,曲晓璐,王小玉,等.维持性血液透析患者慢性肾脏病-矿物质与骨异常的单中心横断面研究[J].中国血液净化,2016,15(10):536-539.[3]Izzo C,Secondulfo C,Bilancio G,et al.Chronic Kidney Disease with Mineral Bone Disorder and Vascular Calcification: An Overview[J].Life (Basel),2024,14(3):418.[4]Nakagawa Y,Komaba H.Roles of Parathyroid Hormone and Fibroblast Growth Factor 23 in Advanced Chronic Kidney Disease[J].Endocrinol Metab (Seoul),2024,39(3):407-415.[5]Nakai K,Kawato T,Morita T,et al.Angiotensin Ⅱ suppresses osteoblastic differentiation and mineralized nodule formation via AT1 receptor in ROS17/2.8 cells[J].Arch Med Sci,2015,11(3):628-637.[6]郭云山,郝定均,刘海平,等.STIM1调控Ras信号通路促进成骨细胞增殖的研究[J].实用骨科杂志,2019,25(10):906-911.[7]Li Y,Shen G,Yu C,et al.Angiotensin Ⅱ induces mitochondrial oxidative stress and mtDNA damage in osteoblasts by inhibiting SIRT1–FoxO3a–MnSOD pathway[J].Biochem Biophys Res Commun,2014,455(1-2):113-118.[8]Zhao Z,Zhang Y,Wang C,et al.Angiotensin Ⅱ upregulates RANKL/NFATC1 expression in synovial cells from patients with rheumatoid arthritis through the ERK1/2 and JNK pathways[J].J Orthop Surg Res,2021,16(1):297.[9]Gupta M,Cheung CL,Hsu YH,et al.Identification of homogeneous genetic architecture of multiple genetically correlated traits by block clustering of genome-wide associations[J].J Bone Miner Res,2011,26(6):1261-1271.[10]Mo C,Ke J,Zhao D,et al.Role of the renin-angiotensin-aldosterone system in bone metabolism[J].J Bone Miner Metab,2020,38(6):772-779.[11]Xie D,Zhao L,Wu L,et al.The levels of bone turnover markers and parathyroid hormone and their relationship in chronic kidney disease[J].Clin Chim Acta,2023,548:117518.[12]Schini M,Vilaca T,Gossiel F,et al.Bone Turnover Markers: Basic Biology to Clinical Applications[J].Endocr Rev,2023,44(3):417-473.[13]Cavalier E,Lukas P,Bottani M,et al.European Biological Variation Study (EuBIVAS): within- and between-subject biological variation estimates of β-isomerized C-terminal telopeptide of type I collagen (β-CTX), N-terminal propeptide of type I collagen (PINP), osteocalcin, intact fibroblast growth factor 23 and uncarboxylated-unphosphorylated matrix-Gla protein-a cooperation between the EFLM Working Group on Biological Variation and the International Osteoporosis Foundation-International Federation of Clinical Chemistry Committee on Bone Metabolism[J].Osteoporos Int,2020,31(8):1461-1470.[14]Ketteler M,Block GA,Evenepoel P,et al.Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder: Synopsis of the Kidney Disease: Improving Global Outcomes 2017 Clinical Practice Guideline Update[J].Ann Intern Med,2018,168(6):422-430.[15]魏雅楠,苗懿德,刘忠厚,等.骨代谢生化标志物的临床进展——不同国家和地区绝经前后女性骨代谢标志物参考值回顾分析[J].中国骨质疏松杂志,2007,13(7):455-468.[16]葛益飞,杨光,王宁宁,等.继发性甲状旁腺功能亢进患者甲状旁腺切除术后骨代谢标志物的短期变化[J].中国血液净化,2018,17(9):588-592.[17]Zhang L,Yu Q,Chen X,et al.Mineral and bone disorder biomarkers and inflammation indexes in patients with end stage renal disease[J].Ann Palliat Med,2020,9(6):3938-3946.[18]Zheng MH,Li FX,Xu F,et al.The Interplay Between the Renin-Angiotensin-Aldosterone System and Parathyroid Hormone[J].Front Endocrinol (Lausanne),2020,11:539.[19]Villa-Etchegoyen C,Lombarte M,Matamoros N,et al.Mechanisms Involved in the Relationship between Low Calcium Intake and High Blood Pressure[J].Nutrients,2019,11(5):1112.[20]Yang T,He M,Zhang H,et al.L- and T-type calcium channels control aldosterone production from human adrenals[J].J Endocrinol,2020,244(1):237-247.

更新日期/Last Update: 1900-01-01