Abstract
The kidney plays an important role in systemic acid–base balance by maintaining the blood HCO3− concentration within narrow limits. Various H+/base transport processes and metabolic pathways have evolved that orchestrate in a coordinated fashion, the absorption of the filtered bicarbonate load and the generation of new HCO3−. The impairment of either of these processes in the nephron can result in a decrease in the blood HCO3− concentration with concomitant metabolic acidosis. In the renal proximal tubule and the collecting duct, secretion of protons by the vacuolar H+-ATPase is one of the key transport steps involved in both the reclamation of filtered HCO3− and the generation of new HCO3−. The activity of the vacuolar H+-ATPase is dynamically regulated by various local and systemic factors. Naturally occurring mutations in specific subunits of the vacuolar H+-ATPase cause the disease distal renal tubular acidosis.
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