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循环补体激活与高血压肾损伤的关系:一项病例对照研究。

Association between circulatory complement activation and hypertensive renal damage: a case-control study.

机构信息

Department of Physical Examination Center, Hebei General Hospital, Shijiazhuang, Hebei, China.

Department of Geriatric Cardiology, Hebei General Hospital, Shijiazhuang, Hebei, China.

出版信息

Ren Fail. 2024 Dec;46(2):2365396. doi: 10.1080/0886022X.2024.2365396. Epub 2024 Jun 14.

DOI:10.1080/0886022X.2024.2365396
PMID:38874150
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11182054/
Abstract

OBJECTIVE

The aim of this study was to investigate the potential importance of complement system activation, with particular emphasis on the complement alternative pathway (AP), in the pathogenesis of hypertensive renal damage.

METHODS

Serum complement C3, complement Factor H (CFH) and AP activation were assessed in 66 participants with established essential hypertension with renal damage (RD). Fifty-nine patients with age- and sex-matched essential hypertension without renal damage (NRD) and 58 healthy participants (normal) were selected.

RESULTS

Our study revealed that C3 and AP50 continuously increased from normal to NRD to RD ( < 0.05, respectively), while CFH was significantly lower than that in NRD and healthy participants ( < 0.05, respectively). After multifactorial logistic regression analysis corrected for confounders, elevated serum C3 ( = 0.001) and decreased CFH ( < 0.001) were found to be independent risk factors for hypertension in healthy participants; elevated serum C3 ( = 0.034), elevated AP50 ( < 0.001), decreased CFH ( < 0.001), increased age ( = 0.011) and increased BMI ( = 0.013) were found to be independent risk factors for the progression of hypertension to hypertensive renal damage; elevated serum C3 ( = 0.017), elevated AP50 ( = 0.023), decreased CFH ( = 0.005) and increased age ( = 0.041) were found to be independent risk factors for the development of hypertensive renal damage in healthy participants.

CONCLUSION

Abnormal activation of complement, particularly complement AP, may be a risk factor for the development and progression of hypertensive renal damage.

摘要

目的

本研究旨在探讨补体系统激活,特别是补体替代途径(AP)在高血压肾损伤发病机制中的潜在重要性。

方法

评估了 66 例已确诊的高血压合并肾损伤(RD)患者、59 例年龄和性别匹配的高血压无肾损伤(NRD)患者和 58 例健康对照者(正常)的血清补体 C3、补体因子 H(CFH)和 AP 激活情况。

结果

本研究显示,C3 和 AP50 从正常到 NRD 再到 RD 呈连续升高(均 < 0.05),而 CFH 显著低于 NRD 和健康对照组(均 < 0.05)。经多因素 logistic 回归分析校正混杂因素后,发现血清 C3 升高( = 0.001)和 CFH 降低( < 0.001)是健康人群高血压的独立危险因素;血清 C3 升高( = 0.034)、AP50 升高( < 0.001)、CFH 降低( < 0.001)、年龄增加( = 0.011)和 BMI 增加( = 0.013)是高血压进展为高血压肾损伤的独立危险因素;血清 C3 升高( = 0.017)、AP50 升高( = 0.023)、CFH 降低( = 0.005)和年龄增加( = 0.041)是健康人群高血压肾损伤发展的独立危险因素。

结论

补体异常激活,特别是补体 AP,可能是高血压肾损伤发生和进展的危险因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8ce/11182054/370be8bf32dc/IRNF_A_2365396_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8ce/11182054/4973ba50d58a/IRNF_A_2365396_F0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8ce/11182054/462609e4defe/IRNF_A_2365396_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8ce/11182054/370be8bf32dc/IRNF_A_2365396_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8ce/11182054/4973ba50d58a/IRNF_A_2365396_F0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8ce/11182054/462609e4defe/IRNF_A_2365396_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8ce/11182054/370be8bf32dc/IRNF_A_2365396_F0003_B.jpg

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Disruption of CXCR6 Ameliorates Kidney Inflammation and Fibrosis in Deoxycorticosterone Acetate/Salt Hypertension.阻断 CXCR6 可减轻血管紧张素Ⅱ诱导的高血压大鼠肾脏炎症和纤维化
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Author Correction: Immune system deregulation in hypertensive patients chronically RAS suppressed developing albuminuria.作者更正:长期肾素-血管紧张素系统(RAS)受抑制的高血压患者免疫系统失调并发展为蛋白尿。
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