Distal renal tubular acidosis has been thought to be the consequence of an impaired ability to maintain a large pH gradient between distal nephron urine and blood. Recent evidence suggests that the classification of deranged distal nephron acidification requires expansion. These mechanisms whereby the urine is acidified in the distal nephron include an active component, a passive component, and a component of bicarbonate secretion. Active proton secretion is influenced by the integrity of the pump and the nature of the electrical chemical gradient against which it operates. The passive component relates either to the backleak of acid from lumen to blood or the leak of bicarbonate from blood to lumen; under ordinary circumstances this passive component is negligible. Aldosterone also influences distal acidification. A defect in most of these components can be identified experimentally. We propose a classification of deranged distal acidification that will allow identification of the mechanism responsible for the defect. This classification, which employs measurement of the urinary carbon dioxide gradient, the response of the kidney to sulfate or phosphate administration, the urinary pH during acidosis, and the state of potassium and sodium excretion, can easily be performed in human subjects.