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炎症细胞因子与高血压危象患者较低的肾小球滤过率相关。

Inflammatory cytokines are associated to lower glomerular filtration rate in patients with hypertensive crisis.

作者信息

Andrade Days O, Aguiar Franciana L, Mansor Ana Luiza P, Valente Flavia M, Souza Doroteia R S, Lopes Valquiria da Silva, Fernandes Leticia B, Godoy Moacir F, Yugar-Toledo Juan C, Cosenso-Martin Luciana N, Vilela-Martin Jose F

机构信息

Hypertension Clinical and Medicine Department, State Medical School at São José do Rio Preto, São Paulo, Brazil.

Biochemistry and Molecular Biology Research Nucleus and Molecular Biology Department, State Medical School at São José do Rio Preto, São Paulo, Brazil.

出版信息

Front Cardiovasc Med. 2022 Sep 29;9:969339. doi: 10.3389/fcvm.2022.969339. eCollection 2022.

DOI:10.3389/fcvm.2022.969339
PMID:36247461
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9559728/
Abstract

INTRODUCTION

Hypertension and kidney function are closely related. However, there are few studies on renal function during acute elevation of blood pressure (BP), denominated hypertensive crisis (HC).

OBJECTIVES

To evaluate the relationship between renal function and inflammatory cytokines in HC, subdivided into hypertensive urgency (HUrg) and emergency (HEmerg).

MATERIALS AND METHODS

This cross-sectional study was carried out in 74 normotensive (NT) and 74 controlled hypertensive individuals (ContrHT) followed up in outpatient care. Additionally, 78 subjects with hypertensive emergency (HEmerg) and 50 in hypertensive urgency (HUrg), attended in emergency room, were also evaluated. Hypertensive crisis was classified into HEmerg, defined by systolic blood pressure (BP) ≥ 180 mmHg and/or diastolic BP ≥ 120 mmHg in presence of target-organ damage (TOD), and HypUrg, clinical situation with BP elevation without TOD. The glomerular filtration rate (eGFR) was estimated, and cytokine levels were measured. Statistical analysis was performed using the Kruskal-Wallis or Mann-Whitney test and Spearman's correlation, with significant differences -value < 0.05.

RESULTS

The median age was 53.5 years in the NT group (52 female), 61 years in the ContrHT group (52 female), and 62.5 years in the HC group (63 female) (-value < 0.0001). The median BP was 118.5/75 mmHg for NT, 113.5/71 for ContrHT, and 198.5/120 mmHg for HC, respectively (-value < 0.0001 among groups). BP and heart rate levels were significantly higher in the HC group compared to the NT and ContrHT groups ( < 0.001 for all). The eGFR was significantly lower in HC group compared to the NT and ContrHT groups. The cytokine levels were higher in the HEmerg and HUrg groups compared to ContrHT group ( < 0.0001, except for IL-1β in HUrg vs. ContrHT), without difference between the acute elevation of BP groups. Thus, all cytokines were significantly elevated in patients with HC compared to the control groups (NT and ContrHT). There was a negative correlation between eGFR and the cytokines (IL-1β, IL-6, IL-8, IL-10, and TNF-α) in the HC group.

CONCLUSION

Elevated inflammatory cytokines are associated with reduced eGFR in individuals with HC compared to control groups, suggesting that the inflammatory process participates in the pathogenesis of acute elevations of BP.

摘要

引言

高血压与肾功能密切相关。然而,关于血压(BP)急性升高(即高血压危象,HC)期间肾功能的研究较少。

目的

评估高血压危象(分为高血压急症,HUrg,和高血压亚急症,HEmerg)中肾功能与炎性细胞因子之间的关系。

材料与方法

本横断面研究纳入了74名血压正常(NT)个体和74名接受门诊随访的血压控制良好的高血压患者(ContrHT)。此外,还对78名在急诊室就诊的高血压亚急症(HEmerg)患者和50名高血压急症(HUrg)患者进行了评估。高血压危象分为高血压亚急症,定义为收缩压(BP)≥180 mmHg和/或舒张压BP≥120 mmHg且伴有靶器官损害(TOD),以及高血压急症,即血压升高但无TOD的临床情况。估算肾小球滤过率(eGFR)并测量细胞因子水平。使用Kruskal-Wallis或Mann-Whitney检验以及Spearman相关性进行统计分析,差异有统计学意义 - 值<0.05。

结果

NT组的中位年龄为53.5岁(女性52名),ContrHT组为61岁(女性52名),HC组为62.5岁(女性63名)(-值<0.0001)。NT组的中位血压为118.5/75 mmHg,ContrHT组为113.5/71 mmHg,HC组为198.5/120 mmHg,组间差异有统计学意义(-值<0.0001)。与NT组和ContrHT组相比,HC组的血压和心率水平显著更高(所有比较均<0.001)。与NT组和ContrHT组相比,HC组的eGFR显著更低。与ContrHT组相比,HEmerg组和HUrg组的细胞因子水平更高(<0.0001,HUrg组与ContrHT组比较时IL-1β除外),血压急性升高组之间无差异。因此,与对照组(NT和ContrHT)相比,HC患者的所有细胞因子均显著升高。HC组中eGFR与细胞因子(IL-1β、IL-6、IL-8、IL-10和TNF-α)之间存在负相关。

结论

与对照组相比,高血压危象患者中炎性细胞因子升高与eGFR降低相关,提示炎症过程参与了血压急性升高的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adda/9559728/779c0b747465/fcvm-09-969339-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adda/9559728/91d97e068f9d/fcvm-09-969339-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adda/9559728/779c0b747465/fcvm-09-969339-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adda/9559728/91d97e068f9d/fcvm-09-969339-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adda/9559728/779c0b747465/fcvm-09-969339-g002.jpg

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