LAUSR

The renoprotective effect through the tubuloglomerular feedback mechanism (TGF) with the Sodium-glucose cotransporter2 inhibitor (SG) attracts attention. We investigated whether the improvement of TGF can be estimated from urinary glucose (UG) and urinary sodium (UNa) excretion, and from other parameters by assessing the changes of urinary findings in patients using SG (Dapagliflozin, Canagliflozin, Empagliflozin). Type 2 diabetes patients with SG who UG and UNa excretion were measured regularly were enrolled in this study. To correct for a postprandial increase of UG due to elevated plasma glucose(PG) levels, the creatinine-corrected UG (cUG: mg/mgCr) was calculated as follows. (The average PG level (AG mg/dl) = 28.7 × HbA1c- 46.7 (Diabetes Care 2008 Aug; 31(8): 1473-1478), the estimated UG (eUG) = UG × AG/PG). Then cUG was corrected for urinary creatinine excretion.) We analyzed these data at before, after 1, 3, 6, and 12 months (M) of SG treatment. Eighteen patients (14 men and 4 women, aged 54.9 ± 6.9 years, eGFR > 100 in 3 and 100. eGFR was negatively correlated with the UNa/cUG ratio and UA(p Disclosure C. Watanabe: None. Y. Mori: None.