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SGLT2 Inhibition and Kidney Potassium Homeostasis.
Palmer, Biff F; Clegg, Deborah J.
Affiliation
  • Palmer BF; Division of Nephrology, Department of Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
  • Clegg DJ; Texas Tech Health Sciences Center, El Paso, Texas.
Clin J Am Soc Nephrol ; 19(3): 399-405, 2024 03 01.
Article in En | MEDLINE | ID: mdl-37639260
Pharmacologic inhibition of the sodium-glucose transporter 2 (SGLT2) in the proximal tubule brings about physiologic changes predicted to both increase and decrease kidney K + excretion. Despite these effects, disorders of plasma K + concentration are an uncommon occurrence. If anything, these drugs either cause no effect or a slight reduction in plasma K + concentration in patients with normal kidney function but seem to exert a protective effect against hyperkalemia in the setting of reduced kidney function or when given with drugs that block the renin-angiotensin-aldosterone axis. In this review, we discuss the changes in kidney physiology after the administration of SGLT2 inhibitors predicted to cause both hypokalemia and hyperkalemia. We conclude that these factors offset one another, explaining the uncommon occurrence of dyskalemias with these drugs. Careful human studies focusing on the determinants of kidney K + handling are needed to fully understand how these drugs attenuate the risk of hyperkalemia and yet rarely cause hypokalemia.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Hyperkalemia / Hypokalemia Type of study: Prognostic_studies Limits: Humans Language: En Journal: Clin J Am Soc Nephrol Journal subject: NEFROLOGIA Year: 2024 Document type: Article Country of publication: United States

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Hyperkalemia / Hypokalemia Type of study: Prognostic_studies Limits: Humans Language: En Journal: Clin J Am Soc Nephrol Journal subject: NEFROLOGIA Year: 2024 Document type: Article Country of publication: United States