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透析液镁与维持性血液透析患者的冠状动脉钙化、骨矿物质密度及痉挛:一项准实验研究

Dialysate Magnesium and Coronary Artery Calcification, Bone Mineral Density, and Cramping in Maintenance Hemodialysis: A Quasi-experimental Study.

作者信息

Srisuwarn Praopilad, Sethakarun Sethanant, Nongnuch Arkom, Jongjirasiri Sutipong, Sritara Chanika, Klyprayong Pinkeaw, Disthabanchong Sinee

机构信息

Division of Nephrology, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.

Bhumirajanagarindra Kidney Institute, Bangkok, Thailand.

出版信息

Kidney Med. 2021 Oct 12;4(2):100374. doi: 10.1016/j.xkme.2021.08.009. eCollection 2022 Feb.

DOI:10.1016/j.xkme.2021.08.009
PMID:35243301
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8861968/
Abstract

RATIONALE & OBJECTIVE: Recent evidence suggests a role for magnesium as a calcification inhibitor. Increased magnesium abundance may attenuate vascular calcification and promote bone formation.

STUDY DESIGN

Parallel-group, 1:1-allocation-ratio, quasi-experimental study.

SETTING & PARTICIPANTS: The study was conducted at hemodialysis centers in Bangkok, Thailand. Patients receiving maintenance hemodialysis were screened for coronary artery calcification (CAC) and bone mineral density (BMD), and those with a CAC score of ≥300 were included and matched according to the initial CAC score. The intervention and control groups consisted of 20 patients in each arm.

INTERVENTIONS

A high (1.75 mEq/L) or standard (0.7 mEq/L) dialysate magnesium concentration was delivered for 26 weeks.

OUTCOMES

Changes in the CAC score and BMD and the progression of CAC. The safety outcomes included occurrence of cramps recorded as per usual care.

RESULTS

The median CAC score of all patients was 1,792. Serum and ionized magnesium concentrations increased substantially in the high dialysate magnesium group. At the end of the study, the CAC score increased significantly in both the groups, with no significant difference between the groups. The number of participants with CAC progression was comparable between the 2 groups. In exploratory subgroup analyses stratified by the median CAC score, a significant decline in CAC and fewer participants with CAC progression were observed in the subgroup with lower CAC scores that received the high dialysis magnesium concentration. Bone mineral density was largely unchanged in both groups. The number of participants experiencing cramps and the number of episodes of muscle cramps were markedly lower among patients who received the high dialysis magnesium concentration.

LIMITATIONS

The participants had severe vascular calcification at baseline; therefore, the findings might not apply to those with less-established calcification. Moreover, cramps were not systematically ascertained.

CONCLUSIONS

The high dialysis magnesium concentration did not alleviate the progression of CAC or improve BMD in patients with severe calcification receiving hemodialysis; however, muscle cramps were less frequent among those treated with high dialysate magnesium. Further study is required to determine a possible favorable effect of high dialysis magnesium concentration in individuals with mild-to-moderate calcification.

摘要

理论依据与目的

近期证据表明镁具有钙化抑制剂的作用。镁含量增加可能会减轻血管钙化并促进骨形成。

研究设计

平行组、1:1分配比例的准实验研究。

研究地点与参与者

该研究在泰国曼谷的血液透析中心进行。对接受维持性血液透析的患者进行冠状动脉钙化(CAC)和骨矿物质密度(BMD)筛查,纳入CAC评分≥300的患者,并根据初始CAC评分进行匹配。干预组和对照组每组各有20名患者。

干预措施

给予高(1.75 mEq/L)或标准(0.7 mEq/L)透析液镁浓度,持续26周。

研究结果

CAC评分和BMD的变化以及CAC的进展情况。安全结果包括按照常规护理记录的痉挛发生情况。

结果

所有患者的CAC评分中位数为1792。高透析液镁组的血清和离子化镁浓度大幅升高。研究结束时,两组的CAC评分均显著增加,两组之间无显著差异。两组中出现CAC进展的参与者数量相当。在按CAC评分中位数分层的探索性亚组分析中,接受高透析液镁浓度的CAC评分较低亚组中,CAC显著下降,且出现CAC进展的参与者较少。两组的骨矿物质密度基本未变。接受高透析液镁浓度的患者中,经历痉挛的参与者数量和肌肉痉挛发作次数明显较少。

局限性

参与者在基线时存在严重血管钙化;因此,研究结果可能不适用于钙化程度较轻的患者。此外,未系统确定痉挛情况。

结论

高透析液镁浓度并不能缓解接受血液透析的严重钙化患者的CAC进展或改善BMD;然而,高透析液镁治疗的患者肌肉痉挛频率较低。需要进一步研究以确定高透析液镁浓度对轻度至中度钙化个体可能产生的有利影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b77/8861968/beba721a21ac/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b77/8861968/fc4c184e4919/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b77/8861968/9c56752ac7fa/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b77/8861968/8290e60c141b/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b77/8861968/ba332813e1c7/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b77/8861968/beba721a21ac/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b77/8861968/fc4c184e4919/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b77/8861968/9c56752ac7fa/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b77/8861968/8290e60c141b/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b77/8861968/ba332813e1c7/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b77/8861968/beba721a21ac/gr4.jpg

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