LAUSR

The use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) is associated with increase of hemoglobin (Hb) levels and this effect has been related to improvement of tubulointerstitial hypoxia and increase on EPO production. Chronic kidney disease (CKD) associated anemia is mainly due to decreased EPO synthesis. The aim of this study was to assess if the degree of Hb increase induced by SGLT2i is higher on T2DM patients with decreased estimated glomerular filtration rate (eGFR). We analyzed the changes on Hb after 12 months of SGLT2i treatment in T2DM patients with different degrees of eGFR. All patients were on maximum tolerated RAA system blockade, and none was on erythropoiesis or iron therapy. 62 patients were include, age 67,6 ± 12,3 years, 72.6% males, eGFR CKD EPI 62,9 ± 21 (21-108) ml/min/1.73m2. Type of SGLT2i was dapagliflozin (46.8%), canagliflozin (30,5%) and empagliflozin (22,6%). 7 patients discontinued SGLT2i therapy and 62 were finally include in the analysis. Treatment with SGLT2i induced increase of Hb levels ( ΛHb 0,57 mg/dl SE 0,17 95% CI 0,25-0,93, p 0,001) independently of eGFR (aR2 0.02 p ns) In the multivariate analysis, initial eGFR, and basal Hb were the main determinants of the Hb increase induced by SGLT2i treatment (aR2 0,29). eGFR (≤60 vs >60 ml/min/173) or type of SGLT2i did not modified ΛHb We conclude that SGLT2 inhibitors induce increase on Hb level independently of eGFR, in patients with preserved renal function, by mechanisms that are yet to be determined.