In a patient with congestive heart failure, which laboratory finding is most likely due to persistent edema despite furosemide treatment?

In a patient with congestive heart failure (CHF), persistent edema can occur despite the use of diuretics such as furosemide. This can be attributed to several compensatory mechanisms that the body activates in response to decreased cardiac output and fluid overload. One of the significant hormonal responses is an increase in plasma aldosterone concentration.

Aldosterone is a hormone produced by the adrenal glands that promotes sodium retention in the kidneys. In CHF, when the effective circulating blood volume decreases due to poor cardiac output, the body senses this as a decrease in perfusion. As a compensatory mechanism, the renin-angiotensin-aldosterone system (RAAS) is activated, leading to increased renin release, which ultimately stimulates the production of aldosterone. The elevation of aldosterone levels contributes to sodium and water retention, exacerbating edema despite treatment with furosemide, which works primarily by increasing urine output to remove excess fluid. Therefore, high plasma aldosterone concentration is a common finding in CHF patients with persistent edema as it represents this compensatory response.

Considering the other options further contextualizes why they are less relevant in this scenario. High serum cortisol concentration could occur due to stress or chronic illness but is not directly linked to the retention