Urine chloride trajectory and relationship with diuretic response in acute heart failure.

IF 3.2 2区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS ESC Heart Failure Pub Date : 2024-10-22 DOI:10.1002/ehf2.15054
Mateusz Guzik, Robert Zymliński, Piotr Ponikowski, Jan Biegus
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Abstract

Aims: Sodium excretion is a well-defined marker used to assess diuretic response in acute heart failure (AHF). Despite a strong pathophysiological background, the role of urine chloride excretion has not been described and established yet. We aimed to evaluate chloride trajectory during intensive diuretic treatment in AHF patients and examine its potential role in predicting poor diuretic response.

Methods: The study was conducted on 50 AHF patients. Participants were included within the first 36 h of hospitalization. They received furosemide dose adjusted for body weight (half in bolus, half in 2 h infusion). Post-diuretic hourly urine collection with biochemical analysis was performed.

Results: In general, the concentrations of urine chloride (uCl-) and sodium (uNa+) at the baseline samples exhibited a comparable level (71 ± 39 vs. 70 ± 44 mmol/L, respectively; P = 0.99), but across all post-furosemide study timepoints, uCl- remained significantly higher than uNa+ since 1 to 6 h of the study. In this course, both ions (uCl- and uNa+) reached peak values in 2 h (114 ± 28 vs. 97 ± 34 mmol/L, respectively; P < 0.01). The pattern of uCl- dominance over uNa+ concentration was also observed in separate analyses of patients naïve to furosemide and those chronically exposed to furosemide. Regardless of these patterns, naïve to furosemide individuals excreted more ions (both uCl- and uNa+) than chronically exposed patients at all timepoints. Additionally, a strong, linear correlation between uCl- and uNa+ was observed in each post-furosemide timepoint (the strongest in 1 h r = 0.87; P < 0.001). Both interdependent ions concentration was almost parallel when analysed in chronic furosemide users and those naïve to furosemide separately [uCl- = 0.85 * uNa+ + 28.82, P < 0.001, R2 = 0.83 for chronic furosemide users, and uCl- = 0.72 * uNa+ + 41.55, P < 0.001, R2 = 0.65 for naïves to furosemide (linear regression model)]. Moreover, uCl- (with cutoff point: 72 mmol/L) was a satisfactory predictive factor for poor diuretic response (<100 mL/h in 6 h since the beginning of furosemide infusion) [odds ratio (OR) 95% confidence interval (CI): 39.0 (3.8-405.00)]. It presented those properties also after adjusting for urine creatinine [cutoff point: 0.296 mmol/mg-OR (95% CI): 81.0 (8.0-816.0)].

Conclusions: Urine chloride and sodium are highly interrelated during decongestion of AHF patients. The uCl- (cutoff 72 mmol/L) exhibits better prognostic abilities to identify poor diuretic response than uNa+.

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急性心力衰竭患者尿氯化物的变化轨迹及其与利尿剂反应的关系。
目的:钠排泄量是一个明确的指标,用于评估急性心力衰竭(AHF)患者对利尿剂的反应。尽管有强大的病理生理学背景,但尿液氯化物排泄的作用尚未被描述和确定。我们旨在评估急性心力衰竭患者在强化利尿剂治疗期间的氯化物排泄轨迹,并研究其在预测不良利尿剂反应方面的潜在作用:研究对象为 50 名 AHF 患者。研究对象为 50 名 AHF 患者。他们接受了根据体重调整的呋塞米剂量(一半为栓剂,一半为 2 小时输注)。尿后每小时收集尿液并进行生化分析:一般来说,基线样本的尿液氯离子(uCl-)和钠离子(uNa+)浓度水平相当(分别为 71 ± 39 mmol/L 和 70 ± 44 mmol/L;P = 0.99),但在呋塞米治疗后的所有研究时间点上,uCl-自研究开始 1 到 6 小时一直显著高于 uNa+。在这一过程中,两种离子(uCl- 和 uNa+)都在 2 小时内达到峰值(分别为 114 ± 28 mmol/L 和 97 ± 34 mmol/L;P - uNa+浓度高于uCl-浓度的情况也在对未使用呋塞米的患者和长期接触呋塞米的患者进行的单独分析中观察到。无论这些模式如何,在所有时间点上,未使用呋塞米的患者都比长期接触呋塞米的患者排出更多的离子(uCl- 和 uNa+)。此外,在呋塞米治疗后的每个时间点,都观察到 uCl- 和 uNa+ 之间存在很强的线性相关(1 小时内 r = 0.87;P - = 0.85 * uNa+ + 28.82,P 2 = 0.83,慢性呋塞米使用者;uCl- = 0.72 * uNa+ + 41.55,P 2 = 0.65,呋塞米新使用者(线性回归模型))]。此外,uCl-(临界点:72 毫摩尔/升)是预测利尿剂不良反应的令人满意的因素(结论:在对 AHF 患者进行去充血治疗时,尿液中的氯和钠密切相关。与 uNa+ 相比,uCl-(截断点:72 毫摩尔/升)在识别不良利尿剂反应方面表现出更好的预后能力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
ESC Heart Failure
ESC Heart Failure Medicine-Cardiology and Cardiovascular Medicine
CiteScore
7.00
自引率
7.90%
发文量
461
审稿时长
12 weeks
期刊介绍: ESC Heart Failure is the open access journal of the Heart Failure Association of the European Society of Cardiology dedicated to the advancement of knowledge in the field of heart failure. The journal aims to improve the understanding, prevention, investigation and treatment of heart failure. Molecular and cellular biology, pathology, physiology, electrophysiology, pharmacology, as well as the clinical, social and population sciences all form part of the discipline that is heart failure. Accordingly, submission of manuscripts on basic, translational, clinical and population sciences is invited. Original contributions on nursing, care of the elderly, primary care, health economics and other specialist fields related to heart failure are also welcome, as are case reports that highlight interesting aspects of heart failure care and treatment.
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