SGLT-2 inhibitors in portal hypertension-related ascites: A case series and potential insights into pathophysiology
JRAAS - Journal of the Renin-Angiotensin-Aldosterone System, cilt.27, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 27
- Basım Tarihi: 2026
- Doi Numarası: 10.1177/14703203261503228
- Dergi Adı: JRAAS - Journal of the Renin-Angiotensin-Aldosterone System
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, CINAHL, EMBASE, MEDLINE, Health Research Premium Collection (ProQuest)
- Anahtar Kelimeler: pathophysiology of ascites, pathophysiology of cirrhosis, Portal vein thrombosis, RAAS in cirrhosis, RAAS in portal hypertension, SGLT-2 inhibitors in cirrhosis, SGLT-2 inhibitors in portal hypertension, presinusoidal portal hypertension
- Süleyman Demirel Üniversitesi Adresli: Evet
Özet
Background: Researches about the pathophysiology of the ascites in cirrhosis continues to evolve. The underfilling hypothesis is the best-known explanation of ascites formation, but the possible contribution of overfilling has become more attention. Aim: To discuss, in light of the literature, whether the different responses to an SGLT2 inhibitor in patients with ascites of different etiologies may reflect differences in the pathophysiological processes underlying ascites formation. Case series: We present four patients with ascites. Two had grade 3 ascites secondary to noncirrhotic portal vein thrombosis (NCPVT) of different etiologies; the other two had Child-Pugh class B cirrhosis and grade 3 ascites. Each had been receiving furosemide and spironolactone, and dapagliflozin 10 mg was introduced for the management of ascites. In the two patients with NCPVT, ascites regressed after dapagliflozin until it was no longer detectable on physical examination. No clinically detectable ascites recurred during the one-year follow-up. In the patients with cirrhosis, ascites also decreased after dapagliflozin but remained detectable on physical examination. The frequency of paracentesis nevertheless declined. Conclusion: In ascites associated with NCPVT, perhaps the predominant pathophysiological process may be angiotensin II-mediated proximal tubular reabsorption secondary to underfilling. In cirrhosis, overfilling appears to contribute alongside underfilling.