First, the neurohormonal hypothesis of hyperfiltration suggests that activation of the renin-angiotensin-aldosterone system (RAAS) during hyperglycemia triggers vasoconstriction at the efferent renal arteriole.1,5–14 In addition, according to the tubular hypothesis (Figure 1), hyperglycemia-induced overexpression of SGLT2 at the proximal tubule15 increases reabsorption of sodium (Na+) and leads to decreased distal Na+ delivery to the macula densa. Here, SLC5A2 is linked to Hyperglycemia.