糖尿病腎臟病變是導致世界上腎臟衰竭的主要原因，並且在醫療照護體系方面造成了沉重的負擔。腎素－血管張力素－醛固酮系統抑制劑之腎臟保護作用於糖尿病人身上已有明顯的效果呈現，尤其是合併有高血壓的病人更為顯著。鈉－葡萄糖共同轉運器-2抑制劑的主要藥理機轉是藉由抑制腎臟近曲小管對血糖的再吸收，因而增加尿糖的排泄以達到降低血糖的效果。除了降低血糖的效用之外，指標性的腎臟結果試驗顯示，患有蛋白尿和腎臟功能衰竭的患者，無論是否有糖尿病，鈉－葡萄糖共同轉運器-2抑制劑可以藉由一系列機轉來減少引發或加劇蛋白尿的風險。這些機轉包括藉由腎小管腎絲球回饋的恢復來減低腎絲球的內壓；透過減低腎素－血管張力素－醛固酮系統的活化來降低腎絲球的高過濾狀態；改善腎小管的氧合和代謝；抵抗發炎、氧化壓力和纖維化以及透過一利尿效應來降低蛋白尿和腎臟去充血化。許多心血管結果試驗也發現這些藥物具有潛在性腎臟保護作用，無論這些病人是否有糖尿病。本篇綜論分析最近關於鈉－葡萄糖共同轉運器-2抑制劑臨床研究之發現和探討其機轉對於在第二型糖尿病合併有慢性腎衰竭的病人之腎臟保護作用。

Diabetic kidney disease is the leading cause of kidney failure worldwide and places considerable burdens on health-care systems. The renoprotective effects of renin-angiotensin-aldosterone system (RAAS) inhibitors have been demonstrated in patients with diabetes, especially when the patient has hypertension. The major pharmacological action of sodium-glucose cotransporter 2 (SGLT2) inhibitor is inhibition of glucose reabsorption in the renal proximal tubule, thus enhancing urinary glucose excretion and reducing the glucose level. Landmark kidney outcome trials have demonstrated that apart from their glucose-lowering effect, SGLT2 inhibitors reduce the risk of development or worsening of albuminuria through a range of mechanisms in patients with or without diabetes who have albuminuria and declining renal function. These mechanisms include reduction of intraglomerular pressure through restoration of the tubuloglomerular feedback; reduction of glomerular hyperfiltration through decreased activation of the RAAS; improvement of tubular oxygenation and metabolism; protection against inflammation, oxidative stress, and fibrosis; and lowering of albuminuria and renal decongestion through a diuretic effect. Several cardiovascular outcome trials have discovered the potential renoprotective effects of these agents in patients with or without diabetes. This review analyzes the most recent findings from clinical trials and identifies the mechanisms through which SGLT2 inhibitors exert renoprotective effects in patients with type 2 diabetes and chronic kidney disease.