#1868 Dapagliflozin reduces urinary kidney injury biomarkers in chronic kidney disease irrespective of albuminuria level

Abstract Background and Aims The beneficial effects of Sodium-Glucose Cotransporter 2(SGLT2) inhibitor in patients with chronic kidney disease (CKD) with low albuminuria levels have not been established. In this study, we aimed to compare the effects of dapagliflozin on kidney injury biomarkers in patients with CKD stratified by albuminuria level. Method We prospectively enrolled healthy volunteers (HVs) (n = 20) and patients with CKD (n = 54) with and without diabetes mellitus (DM). Patients with CKD were divided into two subgroups by age- and sex-matched according to urinary albumin-creatinine ratio (uACR) levels (300 mg/g and ≥300 mg/g). The CKD group received dapagliflozin 10 mg per day. Urine samples were collected before treatment and after 3 months and 6 months of dapagliflozin. Urinary kidney injury molecule-1 (KIM-1), interleukin-1β (IL-1β), and mitochondrial DNA nicotinamide adenine dinucleotide dehydrogenase subunit-1 (mtND1) copy number were measured. Results The estimated glomerular filtration rate (eGFR) of patients with CKD was lower than that of HVs (p 0.001). During the study period, eGFR decreased and uACR did not change in the CKD group. Kidney injury markers were significantly elevated in patients with CKD compared with those in HVs. Dapagliflozin reduced urinary KIM-1, IL-1β and mtDNA copy number in patients with CKD after 6 months of treatment. In further, the levels of urinary KIM-1 and IL-1β, patients with CKD decreased after 6 months of dapagliflozin treatment regardless of albuminuria level. Conclusion In this study, dapagliflozin reduced urinary kidney injury biomarkers in patients with CKD, regardless of albuminuria level. These findings suggest that SGLT2i may also attenuate the progression of low albuminuric CKD.