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1 eneral feature of patients with diabetes and glucosuria.
2 ar glucose transport, resulting in increased glucosuria.
3 ke was entirely explained by the increase in glucosuria.
4 cohort of 60 individuals with familial renal glucosuria.
5 nuria or proteinuria but was associated with glucosuria (1.00 glucosuria vs. 0.19 no glucosuria; P =
6 , as well as in patients with familial renal glucosuria, a condition that is considered a natural mod
8 t mice exhibit a renal Fanconi syndrome with glucosuria and generalized aminoaciduria in addition to
10 ment of salt-induced hypertension by causing glucosuria and natriuresis without changes in the Renin-
11 um-glucose cotransporter-2 inhibitors induce glucosuria and sodium excretion with nephroprotective ef
12 e in urine output and a 500-fold increase in glucosuria, as well as compensatory increases in feeding
14 ubjects with IFG and NFG produces comparable glucosuria but lowers the plasma glucose concentration a
15 SGLT2 (SLC5A2) associate with familial renal glucosuria, but the role of SGLT2 in the kidney is incom
16 ia and effectively normalized hyperglycemia, glucosuria, glucose intolerance, and insulin resistance
17 glycemic effect was associated with a robust glucosuria (> 8 g/dL) observed in nondiabetic mice.
22 se uptake (sum of tissue glucose uptake plus glucosuria) increased in both T2D and NGT following DAPA
26 ening for hypophosphatemia, proteinuria, and glucosuria is recommended for HBV-LT recipients on tenof
27 ical entities defined by the urine dipstick: glucosuria, ketonuria, proteinuria, hematuria and urine
28 Empagliflozin caused 50 +/- 4 and 45 +/- 4 g glucosuria on day 2 in subjects with IFG and NFG, respec
30 the eye phenotype, poor correlation with the glucosuria phenotype did not support a pathogenic role o
32 RC2 alone develop a Fanconi-like syndrome of glucosuria, phosphaturia, aminoaciduria, low molecular w
34 drugs is entirely dependent on the amount of glucosuria produced, it is important to understand why S
38 ects with IFG and NFG, respectively, and the glucosuria was maintained for 2 weeks in both groups.
39 showed significantly more aminoaciduria when glucosuria was present compared with when it was absent