Table 6.

Different mechanisms observed in patients with diabetic mellitus type 1, diabetes mellitus type 2, and nondiabetic chronic kidney disease.

Reference	Proposed different mechanisms
Liu et al.: Cardiorenal protection with SGLT2 inhibitors in patients with diabetes mellitus: from biomarkers to clinical outcomes in heart failure and diabetic kidney disease (36)	Afferent vasoconstriction and efferent vasodilatation. Inflammation markers in patients with type 2 DM treated with SGLT2 inhibitors.
Yoshimoto et al.: Effects of sodium-glucose cotransporter 2 inhibitors on urinary excretion of intact and total angiotensinogen in patients with type 2 diabetes (45)	Angiotensin converting enzyme 2 causing stimulation of the vasodilating and anti-inflammatory alternative pathways, i.e., different balance between angiotensin I (promoting vasoconstriction) and angiotensin 1-7 (promoting vasodilatation)
Hou et al.: Molecular Mechanisms of SGLT2 Inhibitor on Cardiorenal Protection (59)	Arteriole constriction by adenosine and efferent arteriole dilatation by prostaglandins
Schnell et al.: Comparison of mechanisms and transferability of outcomes of SGLT2 inhibition between type 1 and type 2 diabetes (62)	Angiotensin converting enzyme 2 causing stimulation of the vasodilating and anti-inflammatory alternative pathways.
Oguz et al.: Inhibition of sodium glucose cotransporter 2 to slow the progression of chronic kidney disease (82)	Restoration of tubuloglomerular feedback including ketogenesis, renal tissue oxygenation, inflammation, fibrosis