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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.
An initial decline in estimated glomerular filtration rate (eGFR) greater than 10% is not uncommon following sodium–glucose cotransporter 2 inhibitor (SGLT2i) therapy and has been considered a benign or even beneficial effect in clinical trials. This initial eGFR decline is primarily attributed to glucosuria-induced natriuresis, which reduces glomerular hyperfiltration. However, in clinical practice, a subset of SGLT2i users exhibit minimal or absent glucosuria, and the clinical significance of this phenomenon remains unclear. We hypothesized that the absence of glucosuria following SGLT2i therapy is associated with a lower risk of initial eGFR decline.
We established a retrospective cohort of 785 patients aged 18–89 years who were newly prescribed SGLT2 inhibitors between 2015 and 2021 at a tertiary medical center in central Taiwan. Patients with end-stage kidney disease, recent nephrotoxic exposure (within ±90 days), missing serum creatinine data, or SGLT2i use for less than 80% of the initial 90-day period were excluded. Those lacking urine dipstick glucose measurements within 1 year after SGLT2i initiation or showing urine glucose ≥2+ within 1 year before initiation were also excluded. We categorized patients into binary groups based on whether eGFR declined within the first three months after SGLT2i initiation. The primary exposure was defined based on urine dipstick glucose results (1+ or absent) obtained within 1 year after, and closest to, the initiation of SGLT2i therapy. The association between absence of glucosuria and initial eGFR decline was evaluated using multivariable logistic regression.
The median age was 60.8 years (IQR, 50.3–68.7); 93.3% had diabetes, and 18.5% had chronic kidney disease (CKD). A total of 107 patients (13.6%) exhibited absence of glucosuria following SGLT2i use. Compared with those exhibiting significant glucosuria, these patients were more likely to be male, had higher body mass index (BMI), and were more frequently treated with angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), and diuretics. The mean eGFR was 84.1 mL/min/1.73 m² among patients with significant glucosuria and 78.2 mL/min/1.73 m² among those without. A total of 497 patients (63.3%) experienced an initial eGFR decline following SGLT2i therapy. In a multivariable logistic regression model adjusting for age, sex, BMI, and use of ACEIs/ARBs and diuretics, the adjusted odds ratio for initial eGFR dip among patients without glucosuria was 0.58 (95% CI, 0.37–0.90; p = 0.016).
The absence of glucosuria may reflect reduced efficacy of the sodium–glucose co-transporter blockade under SGLT2i therapy, resulting in a missed opportunity to lower glomerular hyperfiltration. This finding suggests potential heterogeneity in SGLT2i responsiveness, and the long-term renal and cardiovascular outcomes of such patients warrant further investigation.
