Diuretics lead to aldosterone excess and hypokalemia by a variety of mechanisms. Diuretic induced volume depletion stimulates the formation of angiotensin II, which, in turn, causes a secondary increase in plasma aldosterone concentration. This increase in plasma aldosterone stimulates potassium excretion, contributing to the hypokalemia. The saline diuresis increased sodium delivery to the collecting tubule. The increased availability of sodium along with the elevated plasma aldosterone augments sodium reabsorption iin the collecting tubule, thereby raising luminal negativity. This high luminal negativity in the collecting tubule promotes secretion of cations, especially hydrogen ions, which raises bicarbonate reabsorption. The saline diuresis causes rapid fluid flow in the distal tubule, which, in turn, keeps luminal potassium concentration low by carrying it away and thus preventing the accumulation of any potassium that enters the lumen. This low luminal concentration of potassium creates a steep concentration gradient for additional potassium losses in the urine. The treatment of edema with thiazide or loop diuretics is the most common cause of metabolic alkalosis. Aerial pH is increased and aerial H+ concentration is decreased with metabolic alkalosis. Sodium depletion tends to decrease plasma sodium levels, although the effect is usually small. Overuse of the thiazide diuretic has caused depletion of sodium and potassium by the kidneys, not retention of sodium and potassium.