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Endogenous sodium-potassium-chloride cotransport inhibitor in congestive heart failure
J L Dubois-Randé1, O Montagne, M Alvarez-Guerra
1INSERM U400, Créteil, France.
Insights
Fluid overload in congestive heart failure (CHF) is linked to increased levels of cotransport inhibitory factor (CIF). This natriuretic factor may help manage fluid overload in CHF patients.
Area of Science:
- Cardiology
- Nephrology
- Endocrinology
Background:
- Humoral mechanisms of volume overload in congestive heart failure (CHF) remain incompletely understood.
- Investigated the potential role of cotransport inhibitory factor (CIF) in the pathophysiology of CHF-related fluid overload.
Purpose of the Study:
- To evaluate the relationship between fluid overload in CHF and cotransport inhibitory factor (CIF).
- To assess CIF as a potential endogenous natriuretic factor in CHF, similar to loop diuretics.
Main Methods:
- Measured plasma and urinary CIF levels in 23 patients with chronic CHF.
- Compared CIF levels with plasma atrial natriuretic peptide (ANP) in CHF patients.
- Utilized 12 healthy individuals without CHF as control subjects.
Main Results:
- CHF patients exhibited a threefold significant increase in plasma CIF and urinary CIF excretion compared to controls (p < 0.0001).
- Elevated CIF levels correlated strongly with impaired left ventricular ejection fraction (r = -0.703, p < 0.0001) and clinical severity.
- Plasma ANP also increased in CHF patients, but to a lesser extent than CIF, and correlated with ejection fraction (r = -0.552, p = 0.0004).
Conclusions:
- Plasma and urinary CIF activities are significantly elevated in chronic CHF.
- CIF, alongside ANP, represents a potential therapeutic agent for managing fluid overload in CHF.
Objectives:
This study sought to evaluate the relation, if any, between fluid overload in congestive heart failure (CHF) and a newly discovered endogenous natriuretic factor acting like loop diuretic drugs: cotransport inhibitory factor (CIF).
Background:
The humoral mechanisms regulating volume overload in CHF are not fully understood. Therefore, we investigated whether there is a role for CIF in this pathologic condition.
Methods:
Plasma and urinary CIF levels were investigated in 23 patients with chronic CHF and compared with changes in plasma atrial natriuretic peptide (ANP). Twelve patients without CHF served as control subjects.
Results:
CHF was associated with a highly significant threefold increase in both plasma CIF levels (mean +/- SD 7.10 +/- 3.01 vs. 2.28 +/- 0.92 U/ml, p < 0.0001) and urinary CIF excretion (7,849 +/- 3,600 vs. 2,351 +/- 1,297 U/day, p < 0.0001) with respect to patients without CHF. CIF increased as a function of impairment in left ventricular ejection fraction (r = -0.703, p < 0.0001) and the severity of clinical status. Plasma ANP was also increased in patients with CHF, although to a lesser extent (68%, p = 0.0501) than plasma CIF, and was also significantly correlated with left ventricular ejection fraction (r = -0.552, p = 0.0004).
Conclusions:
Plasma and urinary CIF activities were strongly and very significantly increased in chronic CHF. In addition to ANP, this long-term natriuretic agent may be of potential importance in reducing fluid overload in CHF.