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IT has long been held that systemic acidemia provides the proximate stimulus for the kidney to increase urinary acidification in response to metabolic acidosis.1 2 3 4 This view has been challenged by the experimental work of Schwartz and associates,5 6 7 8 9 which suggests that the renal acidification response to acid feeding is determined largely, not by acidemia, but by sodium delivery and sodium avidity in the distal nephron. One important implication of this provocative view is that sodium delivery to the distal nephron must be taken into account in the evaluation of normal and altered urinary acidification. Yet, the only criterion required for the . . .
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Batlle et al. (1987) studied this question.
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