Palmer Biff F, Clegg Deborah J
Division of Nephrology, Department of Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Texas Tech Health Sciences Center, El Paso, Texas.
Clin J Am Soc Nephrol. 2024 Mar 1;19(3):399-405. doi: 10.2215/CJN.0000000000000300. Epub 2023 Aug 28.
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.
近端小管中钠-葡萄糖协同转运蛋白2（SGLT2）的药物抑制作用会引发一些生理变化，这些变化预计会同时增加和减少肾脏钾排泄。尽管有这些作用，但血浆钾浓度紊乱并不常见。如果有影响的话，这些药物对肾功能正常的患者要么没有作用，要么会使血浆钾浓度略有降低，但在肾功能减退的情况下，或者与阻断肾素-血管紧张素-醛固酮轴的药物合用时，似乎对高钾血症具有保护作用。在这篇综述中，我们讨论了服用SGLT2抑制剂后预计会导致低钾血症和高钾血症的肾脏生理变化。我们得出结论，这些因素相互抵消，解释了使用这些药物时低钾血症不常见的原因。需要开展针对肾脏钾处理决定因素的严谨人体研究，以全面了解这些药物如何降低高钾血症风险，却很少导致低钾血症。
