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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The preparation of this article was supported in part by funds from the NIH (R01-DK077162), the Allan Smidt Charitable Fund, the Factor Family Foundation, and the Arvey Foundation.
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Kurtz, I., Rogova, I., Turygin, V., Huang, J., Abuladze, N., Pushkin, A. (2016). Renal H+-ATPase Function, Regulation, and Role in Distal Renal Tubular Acidosis. In: Chakraborti, S., Dhalla, N. (eds) Regulation of Ca2+-ATPases,V-ATPases and F-ATPases. Advances in Biochemistry in Health and Disease, vol 14. Springer, Cham. https://doi.org/10.1007/978-3-319-24780-9_25
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