alkalosis, the conservation of chloride is intact, and a urine chloride concentration less than 25 mEq/L would be consistent with volume depletion A urine chloride concentration greater than 40 mEq/L in the setting of metabolic alkalosis would be consistent with disorders such as primary mineralocorticoid excess, Bartter syndrome, Gitelman syndrome, or continued diuretic therapy The treatment of metabolic alkalosis is supportive, and reversible underlying causes should be addressed The focus of therapy should aim at restoring adequate circulating volume and correcting chloride and potassium deficits Providing isotonic sodium chloride will restore intravascular volume, remove the stimulus for sodium retention, and increase distal chloride delivery Once these results have been achieved, there will be decreased bicarbonate reabsorption, increased bicarbonate excretion, and correction of the metabolic alkalosis Potassium chloride should be provided if depletion is suspected with close monitoring to avoid excessive replacement Though the extracellular concentration of potassium may be low during metabolic alkalosis due to transcellular shift to the intracellular space, true potassium depletion may be present Potassium can be lost due to impaired renal absorption from diuretic therapy, aldosterone effect associated with volume depletion, and obligatory wasting of cations (Na+ and K+ ) associated with bicarbonate excretion In patients with metabolic alkalosis and edematous states, providing sodium chloride may be hazardous Therapy should take into account the underlying condition and planned in concert with appropriate subspecialty care if possible ACUTE KIDNEY INJURY CLINICAL PEARLS AND PITFALLS