Background: Sodium-glucose linked transporter 2 inhibitors (SGLT2s) are currently favoured for their tolerability, cardiovascular benefit and renal protective effects. However, due to their mechanism of action, they are only licensed for use in those with preserved renal function at baseline. Previous analyses with other drugs in the class showed potential benefits even when used in those with estimated glomerular filtration rate (eGFR) below licensed level.

Methods: Data was extracted from the ABCD nationwide empagliflozin audit and then stratified into groups, as follows, based on baseline eGFR (mL/min/1.73m2): CKD1 (n=2900, eGFR≥90), CKD2 (n=2753, eGFR<90, eGFR≥60), CKD3a (n=210, eGFR<60, eGFR≥45) and CKD3b+ (n=17, eGFR<45). Data was analysed using paired t-tests and ANOVA in Stata 16.

Results: 5880 datasets were included with mean (±SD) age 59.5yrs (±10.4), 61.1% male, 86% Caucasian (where known), BMI 33.1kg/m2 (±6.6), HbA1c 9.17% (±1.61) and median duration diabetes 7.3 years (2.2-12.1 IQR) and were broadly similar across groups apart from age: those with more impaired renal function being generally older (CKD1 55.4yrs±9.5 v CKD3b+ 69.6yrs±8.5) with a longer duration diabetes with median (IQR) in CKD1 6.6yrs (1.8-10.9) v CKD3b+ 14.5yrs (8.9-17.3). Reductions in HbA1c, weight and BMI occurred in all groups (P<0.005); reductions in HbA1c were of a smaller magnitude as eGFR declined (ANOVA P<0.01). Changes in systolic (SBP) and diastolic blood pressure (DBP) were significant in those in CKD1- CKD3a but not in CKD3b+ (SBP +2.6mmHg, 95% CI +14.9, -9.6). eGFR was observed to decrease in CKD1 and CKD2 (CKD1 eGFR -2.1mL/min/1.73m2, CI 95% -1.8, -2.3).

Conclusion: The use of empagliflozin at eGFR<45mL/min/1.73m2 may still confer HbA1c improvement (although perhaps of lower magnitude) and weight loss, though SBP and DBP reduction may be limited. More evidence is needed regarding its use at lower levels of eGFR.


T.S.J. Crabtree: None. K. Adamson: None. A. Bickerton: None. S.M. Phillips: None. A. Evans: Other Relationship; Self; AstraZeneca. A.M. Robinson: None. M. Atkin: Speaker’s Bureau; Self; AstraZeneca, Napp Pharmaceuticals. D.S. Morris: None. D.M. Williams: None. J.W. Stephens: Speaker’s Bureau; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Napp Pharmaceuticals, Novo Nordisk A/S. D.K. Sennik: Speaker’s Bureau; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Novo Nordisk Inc., Sanofi. A. Rohilla: None. M.L. Cull: None. R.P. Raghavan: Research Support; Self; Allergan plc. Speaker’s Bureau; Self; Abbott, AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Lilly Diabetes, Napp Pharmaceuticals, Takeda UK. Other Relationship; Self; Napp Pharmaceuticals. M. Yadagiri: None. I.W. Gallen: None. R.E. Ryder: Consultant; Self; GI Dynamics Inc. Other Relationship; Self; Novo Nordisk A/S.

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