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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
In the last years the inhibitors of Sodium-Glucose cotransporter type 2 (SGLT2i) have revolutionized the prognosis of diabetic nephropathy. However, many aspects of their effect are unclear, specifically in relation to the paradoxical increase in hemoglobin level observed in many treated patients. Fibroblast-like cells endowed among kidney proximal tubules, known as “Norn cells”, are considered as responsible for oxygen sensing and Epo production. Even though preliminary data suggest an effect of SGLT2i on Norn cells, here we explore the possibility that this effect is mediated by endothelial cells in peritubular spaces (which we have demonstrated to express SGLT2 under stress conditions).
We hypothesize that SGLT2i counteract the inflow of glucose in endothelial cells in diabetic patients, thereby re-establishing their normal thickness.
We have verified the presence of Epo cells at different ages using the Human protein atlas. Immunohistochemical images of Epo on kidney sections were thresholded using SGLT2 staining to establish the cutoff signal. We then performed histological analysis of renal biopsies from diabetic nephropathy (SGLT2i-treated patients n=15; SGLT2i-naïve patients n=15). The control group was matched for age, eGFR, proteinuria and blood pressure to ensure comparable baseline characteristics. Finally, the effects of SGLT2i on hemoglobin levels were confirmed on an independent cohort of 371 patients with CKD. The cohort had a mean age of 65 years and consisted predominantly of males (65%) and Caucasians (98%).
In SGLT2i-treated patients hemoglobin levels showed a statistically significant median increase of 0.40 g/dL (P = 2.63 × 10⁻¹¹). Renal biopsies demonstrated a significant reduction in proximal tubular cell thickness and interstitial cell number that is correlated with serum creatinine in SGLT2i treated. Endothelial morphometry revealed no distinction in cell count or capillary cross-sectional area. However, patients treated with SGLT2i showed a significant decrease of endothelial cell thickness in peritubular capillaries, indexed by the endothelial area fraction, suggestive of reduced endothelial edema.
This study uncovers a novel layer of SGLT2i activity, linking renal microvascular remodeling to hematological improvement in patients with diabetic nephropathy. Beyond their established glycosuric and nephroprotective properties, SGLT2i improve hemoglobin levels through mechanisms independent of traditional erythropoietic stimulation. The observed reduction in endothelial area fraction indicates attenuation of endothelial swelling and improved capillary integrity, suggesting enhanced microcirculatory efficiency. These observations broaden our understanding of SGLT2 inhibitors’ pleiotropic effects and open new therapeutic perspectives for managing the dual challenge of kidney disease and anemia.
