SGLT2 brings glucose in with sodium. The sodium is taken back up (with the glucose but on different transporters) via the sodium potassium exchanger. When you inhibit SGLT2 doesn't bring in sodium and glucose and there isn't sodium to exchange for potassium and thus potassium remains and can get high. This is especially higher risk if combined with potassium sparing diuretics or ACE inhibitors.l or those with renal impairment.
I think it's bc the sheer amount of K+ not secreted into lumen at PCT is far larger than the K+ that'd be excreted at IMCD from RAAS activation. This might be similar in effect to how azetolamide, which indirectly inhibits Na+ reabsorption in PCT, causes hyperkalemia too.
Edit: yeah ignore that last line, I’m totally wrong about acetazolamide’s effecr on serum K+ levels
I think it's bc the sheer amount of K+ not secreted into lumen at PCT is far larger than the K+ that'd be excreted at IMCD from RAAS activation. This might be similar in effect to how azetolamide, which indirectly inhibits Na+ reabsorption in PCT, causes hyperkalemia too.
This site uses cookies to help personalize content, tailor your experience and to keep you logged in if you register.
By continuing to use this site, you are consenting to our use of cookies and terms of service.
