The term 'renal tubular acidosis' (RTA) applies to a group of disorders characterized by nonanion gap metabolic acidosis caused by abnormalities of the renal acidification mechanisms. Failure to thrive is the most prominent clinical feature and it is caused by sustained acidosis. Type 1 RTA is produced by an alteration in some of the distal mechanisms. The acidosis in this case is severe and progressive, is accompanied by hypercalciuria and may be complicated by nephrolithiasis and nephrocalcinosis. Hypokalemia is frequent, except for the 'voltage-dependent' subtype, where there is hyperkalemia. The treatment consists of alkali therapy. Potassium supplements are usually needed in the hypokalemic subtypes. Type 2 RTA is caused by a decrease in proximal bicarbonate reabsorption. It is frequently associated with other proximal tubule abnormalities, such as the Fanconi syndrome, but it may be isolated. Bone disease is frequent. Nephrolithiasis and nephrocalcinosis have not been described. Sodium bicarbonate and potassium supplements are also used for treatment of this type. Type 4 RTA is caused by aldosterone deficiency or resistance. Hyperkalemia is the main clinical feature. Different subtypes have been described. The treatment, again, consists of alkali therapy. In addition, some patients benefit from a high-Na+ diet. Cation exchange resins may be necessary in some cases. Mineralocorticoids are used in cases of hypoaldosteronism.