Which diuretic can lead to metabolic alkalosis due to electrolyte disturbances?

Loop diuretics, such as furosemide and bumetanide, can indeed lead to metabolic alkalosis as a result of electrolyte disturbances. These diuretics are known for their ability to inhibit the sodium-potassium-chloride co-transporter in the thick ascending limb of the loop of Henle. This action increases the excretion of many electrolytes, particularly sodium and chloride, along with significant volumes of water.

The loss of chloride can disrupt the acid-base balance of the body, leading to the development of metabolic alkalosis. When chloride is lost, the kidney attempts to compensate through various mechanisms, including the retention of bicarbonate. As bicarbonate accumulates in the body, the pH of the blood can rise, resulting in a state of alkalosis.

Loop diuretics also cause potassium loss, which can lead to hypokalemia. Hypokalemia can further exacerbate metabolic alkalosis since low potassium levels can increase renal tubular bicarbonate reabsorption, compounding the metabolic alkalosis.

In contrast, thiazide diuretics also cause electrolyte disturbances but tend to lead to different metabolic effects and have a more moderate impact on acid-base balance compared to loop diuretics. Potassium-sparing diuretics are