The study of derangements in salt, water, and acid-base homeostasis frequently reveals much about renal transport mechanisms and their regulation. The study of one such derangement, metabolic alkalosis, has played a special role in contributing to our knowledge of renal function. Elucidation of the kidney's role in the generation, maintenance, and correction of metabolic alkalosis has provided information about proximal tubule transport and its response to volume contraction, volume expansion, and K depletion. Also, distal nephron transport and its response to mineralocorticoids and dietary anion composition have been clarified by studies on metabolic alkalosis. Finally, we have learned about the importance of Na delivery to distal nephron sites and the avidity with which these distal nephron sites reabsorb sodium. Indeed, reviews on the subject of metabolic alkalosis have presented thorough and convincing physiologic arguments on how the kidney helps to generate and maintain this derangement in acid-base balance. However, more recent experimental work has led some to reconsider how the kidney functions in metabolic alkalosis. In an earlier paper in this journal, Galla, Bonduris, and Luke present an argument for the correction of chloride-depletion alkalosis in the rat without volume expansion. In this editorial we discuss their study, summarize the classical features of metabolic alkalosis of primary mineralocorticoid excess as well as metabolic alkalosis associated with volume contraction, and review the results of newer studies, attempting to integrate these two existing models of the kidney's role in the generation, maintenance, and correction of metabolic alkalosis.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - Jan 1 1983|
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