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Vitzthum, H; Koch, M; Eckermann, L; Svendsen, S L; Berg, P; Hübner, C A; Wagner, C A; Leipziger, J; Meyer-Schwesinger, C; Ehmke, H
Nature communications, 05/2023, Letnik: 14, Številka: 1Journal Article
The kidney plays a key role in the correction of systemic acid-base imbalances. Central for this regulation are the intercalated cells in the distal nephron, which secrete acid or base into the urine. How these cells sense acid-base disturbances is a long-standing question. Intercalated cells exclusively express the Na -dependent Cl /HCO exchanger AE4 (Slc4a9). Here we show that AE4-deficient mice exhibit a major dysregulation of acid-base balance. By combining molecular, imaging, biochemical and integrative approaches, we demonstrate that AE4-deficient mice are unable to sense and appropriately correct metabolic alkalosis and acidosis. Mechanistically, a lack of adaptive base secretion via the Cl /HCO exchanger pendrin (Slc26a4) is the key cellular cause of this derailment. Our findings identify AE4 as an essential part of the renal sensing mechanism for changes in acid-base status.
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