It is important to consider the diagnosis of renal tubular acidosis (RTA) when a non-anion-gap metabolic acidosis has a new onset. In RTA, bicarbonate is excreted through the kidneys and chloride ion is reabsorbed, leading to the two major serum characteristics of these syndromes: metabolic acidosis and hyperchloremia. These disorders may be associated with either hypokalemia (types I and II RTA) or hyperkalemia (type IV RTA). The other causes of a hyperchloremic metabolic acidosis include bicarbonate losses through the gastrointestinal tract (e.g., diarrhea or urinary diversions) and an excess administration of chloride, which may occur from excess chloride ion administration. The latter can occur secondary to the large-volume administration of normal saline during resuscitation from trauma or with treatment of diabetic ketoacidosis. In addition, the imbalance can occur with the excess use of chloride salts rather than acetate salts for critically ill patients receiving total parenteral nutrition.