Daniel Fuster
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danfuster.bsky.social
Daniel Fuster
@danfuster.bsky.social
Nephrologist and physician-scientist at Inselspital Bern, Switzerland. Kidney stone and rare kidney disease enthusiast. Passion for climbing, skiing and mountaineering.
Thank you Pedro. Unfortunately not many groups working on these important transporters anymore.
March 29, 2025 at 4:25 PM
Agree. This study shows nicely that it is dose equivalence and not type of thiazide that matters. CTD is ~2x more potent than HCT (and Indapamide ~20x more potent than HCT).
December 15, 2024 at 12:34 PM
Not that I know of - and yes this should be done. Likely indirect effect in PT (as is the case for SGLT2i-mediated inhibition of NHE3), yet direct inhibition cannot be ruled out at this stage. NaDC1 has been a prime target for stone prevention for long-it seems SGLT2is are what we were looking for !
December 11, 2024 at 5:16 AM
No - we were told first two weeks in January 25
December 9, 2024 at 9:47 AM
Many putative mechanisms how RSR CaP can affect CaOx stone formation (Randall, heterogeneous nucleation etc), but also threats ( increase in urine calcium). This is why we need outcome data
December 9, 2024 at 6:30 AM
Went up slightly from 30 to 35 mmol/d.
December 9, 2024 at 6:26 AM
SGLT2is likely inhibit citrate reabsorption in the PT. No need for alkalosis. Urine citrate and pH drove reduction in RSR CaP.
Urine calcium went up in patients with calcium stones, no change in oxalate.
December 9, 2024 at 5:52 AM
Reposted by Daniel Fuster
… and you might even dream (or fool yourself?) about achieving lower sodium intake in your patients, but the most likely explanation for the negative result of #NOSTONE, is just that: Thiazides do not work very well in preventing recurrent kidney stones. 2/2
December 7, 2024 at 10:02 PM