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Neurohormonal Activation and Renal Chloride Avidity in Acute Heart Failure: Clinical Evidence Supporting the

Hajime Kataoka1

  • 1From the Internal Medicine, Nishida Hospital, Oita, Japan.

Cardiorenal Medicine
|January 30, 2024
PubMed

Insights

The "chloride (Cl) theory" for heart failure (HF) suggests serum chloride concentration changes drive HF progression. This study found renal chloride avidity, influenced by neurohormones, plays a key role in acute HF.

Area of Science:

  • Cardiology
  • Nephrology
  • Endocrinology

Background:

  • The "chloride (Cl) theory" proposes that changes in serum chloride concentration ([sCl-]) contribute to heart failure (HF) progression.
  • Understanding the role of neurohormones and renal chloride avidity is crucial for elucidating HF pathophysiology.

Purpose of the Study:

  • To investigate the association between neurohormones and renal chloride avidity in patients with acute HF.
  • To determine the contribution of these factors to acute HF and their involvement in the "Cl theory."

Main Methods:

  • Analysis of blood and urine samples from 29 acute HF patients before treatment.
  • Measurement of electrolytes, b-type natriuretic peptide (BNP), and plasma neurohormones.
  • Categorization of patients into "excretion" (low renal Cl avidity) and "absorption" (high renal Cl avidity) groups based on [sCl-]-[uCl-] difference.

Main Results:

  • Urinary chloride ([uCl-]) inversely correlated with plasma renin activity (PRA) and aldosterone.
  • The [sCl-]-[uCl-] difference positively correlated with PRA and aldosterone.
  • The "absorption" group showed greater renal impairment, higher cardiac burden (BNP), elevated PRA, and lower fractional urinary chloride excretion compared to the "excretion" group.

Conclusions:

  • Renal chloride avidity exhibits distinct types (excretion vs. absorption) in acute HF.
  • Renin-aldosterone-angiotensin activity underlies these differences, providing a neurohormonal basis for the "Cl theory."
  • These findings offer insights into HF pathophysiology and potential therapeutic targets.
Abstract

Keywords:
ChlorideHeart failurePlasma renin activityTubule-glomerular feedback mechanism

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