Abstract
Because majority of biological processes are dependent on pH, maintaining systemic acid-base balance is critical. The kidney contributes to systemic acid-base regulation, by reabsorbing HCO3 − (both filtered by glomeruli and generated within a nephron) and acidifying urine. Abnormalities in those processes will eventually lead to a disruption in systemic acid-base balance and provoke metabolic acid-base disorders. Research over the past 30 years advanced our understanding on cellular and molecular mechanisms responsible for those processes. In particular, a variety of transgenic animal models, where target genes are deleted either globally or conditionally, provided significant insights into how specific transporters are contributing to the renal acid-base regulation. Here, we broadly overview the mechanisms of renal ion transport participating to acid-base regulation, with emphasis on data obtained from transgenic mice models.



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Notes
The actual acid form of this buffer system is not CO2 but rather is carbonic acid H2CO3. However, H2CO3 is rapidly converted into CO2 by carbonic anhydrase and, for the sake of simplicity, we will consider in this review that the acid form is CO2.
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Acknowledgments
D Eladari and coworkers are funded by the Institut National de la Santé et de la Recherche Médicale (INSERM). This work was also funded by grants from l’Agence Nationale de la Recherche (Appel à projet BLANC 2010-HYPERCLO and Appel à Projet Générique 2014-HYPERSCREEN to D.E.).
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Eladari, D., Kumai, Y. Renal acid-base regulation: new insights from animal models. Pflugers Arch - Eur J Physiol 467, 1623–1641 (2015). https://doi.org/10.1007/s00424-014-1669-x
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DOI: https://doi.org/10.1007/s00424-014-1669-x