From the Internal Medicine, Nishida Hospital, Oita, Japan.
Cardiorenal Med. 2024;14(1):94-104. doi: 10.1159/000536293. Epub 2024 Jan 30.
Heart failure (HF) progression according to changes in the serum chloride concentration ([sCl-]) was recently proposed as the "chloride (Cl) theory" for HF pathophysiology. The present study examined the association of neurohormones and renal Cl avidity to determine their contribution to acute HF and their involvement to the "Cl theory."
Data from 29 patients with acute HF (48% men; 80.3 ± 12 years) were analyzed. Blood and urine samples were obtained before decongestive therapy. Clinical tests included peripheral blood, serum and spot urinary electrolytes, b-type natriuretic peptide (BNP), and plasma neurohormones.
In the 29 patients, urinary Cl concentrations ([uCl-]) inversely correlated with log (plasma renin activity [PRA]) (r = -0.64, p = 0.0002) and log (plasma aldosterone concentration) (r = -0.50, p = 0.006). The [sCl-]‒[uCl-] difference positively correlated with log PRA (r = 0.63, p = 0.0002) and log (plasma aldosterone concentration) (r = 0.49, p = 0.008). Patients were divided into 2 groups according to the [sCl-]‒[uCl-] difference, an excretion (low renal Cl avidity) group and an absorption (high renal Cl avidity) group. Compared with the excretion group (-77 to ‒5 mEq/L; n = 14), the absorption group (1-84 mEq/L; n = 15) exhibited greater renal impairment (serum creatinine; 1.45 ± 0.63 vs. 1.00 ± 0.38 mg/d, p = 0.029) and cardiac burden (log BNP; 2.99 ± 0.3 vs. 2.66 ± 0.32 pg/mL, p = 0.008), higher log PRA (0.20 ± 0.58 vs. -0.25 ± 0.35 ng/mL/h, p = 0.018), and lower fractional urinary Cl excretion (1.34 ± 1.3 vs. 5.33 ± 4.1%, p < 0.001).
Renal Cl avidity differs in acute HF, i.e., excretion (low renal Cl avidity) versus absorption (high renal Cl avidity) types, involving renin-aldosterone-angiotensin activity as the underlying mechanism, which provides the neurohormonal background for the "Cl theory." A version of this study was presented in part at the annual international scientific assembly (ACC.23) of the American College of Cardiology, March 4-6, 2023.
心力衰竭（HF）根据血清氯浓度（[sCl-]）的变化而进展，最近被提出作为心力衰竭病理生理学的“氯（Cl）理论”。本研究检查了神经激素和肾脏 Cl 摄取的相关性，以确定它们对急性 HF 的贡献及其对“Cl 理论”的参与。
分析了 29 名急性 HF 患者（48%为男性；80.3±12 岁）的数据。在去充血治疗前采集血液和尿液样本。临床检查包括外周血、血清和尿液电解质、B 型利钠肽（BNP）和血浆神经激素。
在 29 名患者中，尿 Cl 浓度（[uCl-]）与 log（血浆肾素活性 [PRA]）呈负相关（r=-0.64，p=0.0002），与 log（血浆醛固酮浓度）呈负相关（r=-0.50，p=0.006）。[sCl-]-[uCl-]差值与 log PRA 呈正相关（r=0.63，p=0.0002），与 log（血浆醛固酮浓度）呈正相关（r=0.49，p=0.008）。根据[sCl-]-[uCl-]差值将患者分为 2 组，排泄（低肾 Cl 摄取）组和吸收（高肾 Cl 摄取）组。与排泄组（-77 至-5mEq/L；n=14）相比，吸收组（1-84mEq/L；n=15）的肾功能障碍更严重（血清肌酐；1.45±0.63 与 1.00±0.38mg/d，p=0.029）和心脏负担（logBNP；2.99±0.3 与 2.66±0.32pg/mL，p=0.008），更高的 logPRA（0.20±0.58 与-0.25±0.35ng/mL/h，p=0.018）和更低的尿 Cl 排泄分数（1.34±1.3 与 5.33±4.1%，p＜0.001）。
急性 HF 中肾脏 Cl 摄取存在差异，即排泄（低肾 Cl 摄取）型与吸收（高肾 Cl 摄取）型，涉及肾素-血管紧张素-醛固酮系统活性作为潜在机制，为“Cl 理论”提供了神经激素背景。该研究的一个版本在 2023 年 3 月 4 日至 6 日举行的美国心脏病学会（ACC.23）年度国际科学大会上部分展示。
