{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:01:58Z","timestamp":1785542518707,"version":"3.56.0"},"reference-count":77,"publisher":"Portland Press Ltd.","issue":"1","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,2,27]]},"abstract":"<jats:p>Chronic kidney disease (CKD) is characterized by progressive reduction in kidney function and treatments aiming at stabilizing or slowing its progression may avoid or delay the necessity of kidney replacement therapy and the increased mortality associated with reduced kidney function. Metabolic acidosis, and less severe stages of the acid stress continuum, are common consequences of CKD and some interventional studies support that its correction slows the progression to end-stage kidney disease. This correction can be achieved with mineral alkali in the form of bicarbonate or citrate salts, ingestion of diets with fewer acid-producing food components or more base-producing food components, or a pharmacological approach. In this mini-review article, we summarize the potential mechanisms involved in the beneficial effects of alkali therapy. We also discuss the perspectives in the field and challenges that must be overcome to advance our understanding of such mechanisms.<\/jats:p>","DOI":"10.1042\/bst20220690","type":"journal-article","created":{"date-parts":[[2023,2,6]],"date-time":"2023-02-06T11:27:16Z","timestamp":1675682836000},"page":"223-232","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["The mechanisms of alkali therapy in targeting renal diseases"],"prefix":"10.1042","volume":"51","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2805-3601","authenticated-orcid":false,"given":"Pedro Henrique","family":"Imenez Silva","sequence":"first","affiliation":[{"name":"1Institute of Physiology, University of Zurich, Zurich, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donald E.","family":"Wesson","sequence":"additional","affiliation":[{"name":"2Dell Medical School \u2013 The University of Texas at Austin, Austin, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carsten A.","family":"Wagner","sequence":"additional","affiliation":[{"name":"1Institute of Physiology, University of Zurich, Zurich, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2023,2,6]]},"reference":[{"key":"2023022712001165200_","doi-asserted-by":"publisher","first-page":"291","DOI":"10.1016\/S0272-6386(97)90045-7","article-title":"The clinical spectrum of chronic metabolic acidosis: homeostatic mechanisms produce significant morbidity","volume":"29","year":"1997","journal-title":"Am. 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