Which investigation finding would correlate with a low serum potassium level in a patient on furosemide for heart failure?

In patients taking furosemide, a loop diuretic, for heart failure, low serum potassium levels are often observed due to the drug's action on the kidneys, where it inhibits sodium and chloride reabsorption in the ascending loop of Henle. This leads to a subsequent loss of potassium in the urine, resulting in hypokalemia.

When serum potassium levels drop, the body responds by activating the renin-angiotensin-aldosterone system (RAAS) as a compensatory mechanism to retain sodium and potassium. Consequently, there is an increase in plasma aldosterone concentration. Aldosterone promotes sodium reabsorption and potassium excretion in the kidneys, which can exacerbate the existing hypokalemia in patients who are already losing potassium due to the diuretic.

High plasma aldosterone concentration correlates with the body's attempt to compensate for low potassium levels by increasing reabsorption of sodium and further stimulating the excretion of potassium. Thus, this finding aligns well with the low serum potassium observed in these patients on furosemide therapy, making it the most logical choice among the options.

In contrast, low plasma renin concentration or low plasma angiotensin II concentration would suggest a decreased activation of the RAAS and is not