Camillo Tancredi Strizzi

🧵1. Aldosterone isn’t just “salt & water.” In modern sodium-rich contexts it drives inflammation, fibrosis, and residual cardiorenal risk. We map physiology → disease → therapies, and argue for reprogramming the signal. Follow the thread ---> doi.org/10.3390/ijms26…

Now open access in @NDTsocial CKD of unexplained cause (CKDx): A consensus statement by the Genes &Kidney Working Group of the ERA 🧐Check also our 2 open access editorials on this innovative concept. ▶️academic.oup.com/ndt/article/do…

Full paper available in open access, in collaboration with @Violadmb & @FrancescoPesce. @IJMS_MDPI doi.org/10.3390/ijms26…

3. Connecting Tubule/Collecting Duct α-Intercalated cell 🎯 Aldo → H⁺ secretion (H-ATPase/H/K-ATPase) β-Intercalated cell (base/Cl⁻) 🛑Aldo suppresses Pendrin (Cl/HCO₃ handling) 🧪Aldosterone excess contribute to metabolic alkalosis with hypokalemia.

Where does aldosterone actually do its work? In the aldosterone-sensitive distal nephron (ASDN): DCT2, CNT, and the collecting duct. The control room for Na⁺ balance and K⁺ homeostasis. (Follow the thread 🧵) #Nephpearls #Nephrology #Physiology

8. Aldosterone: From Essential Tubular Regulator to Pathological Driver—Physiology, Disease, and Therapeutic Advances. In collaboration with @FrancescoPesce @DAmbrosioViola Open Access in @IJMS_MDPI: doi.org/10.3390/ijms26…

7. Future & biomarkers 🔬 Non-genomic pathways (GPER), NLRP3 blockade, TLR/biglycan axis, miRNA, immune re-balancing and others. 👉The goal: pathway-informed, biomarker-guided precision nephrology.

🧵1. Aldosterone isn’t just “salt & water.” In modern sodium-rich contexts it drives inflammation, fibrosis, and residual cardiorenal risk. We map physiology → disease → therapies, and argue for reprogramming the signal. Follow the thread ---> doi.org/10.3390/ijms26…

The success paradox: better therapies → rarer events → longer, costlier trials. Our proposal: smarter trials, not bigger, use adaptive & pragmatic designs, eGFR slope as surrogate, RWE and continue DHT monitoring. @FrancescoPesce shorturl.at/yEeC3

Proud to share our new paper: a road map to redesign nephrology clinical trials by pairing modern methodology and computational tools. With @FrancescoPesce. shorturl.at/kDg50

Basics of Glomerulonephritis (GN). GBM is key. All patterns can be explained by glomerular basement membrane (GBM) & type of injury. Let’s do one at a time CRESCENTIC GN 1. Results from breach/break of GBM (red arrow) 2. Injury is sudden & severe Eg-ANCA & anti-GBM GN

"Drink more water!" It's the easiest health advice around. Tired? Headache? Trying to be like Tom Brady? Just drink more water. But as a nephrologist, I get asked all the time: How much is the right amount? And the truth is... we don't really know. 🧵

1/14 🤔 Why do we use iodine as an intravenous contrast agent? The answer requires a review of the composition of the human body and a brief tour of one of my favorites, the Periodic Table of Elements.

🚨 Discover how intramolecular epitope spreading in PLA2R-associated Membranous Nephropathy escalates disease severity. As autoantibodies expand from CysR to CTLD domains, inflammation intensifies, driving proteinuria and reducing chances of remission. t.ly/tMLkH