腎小球高過濾狀態使得腎元不可逆地容易受到損傷，因此，在啟動糖尿病慢性腎臟病的發展中扮演一個重要的角色。腎小球高過濾狀態在過去的臨床研究中強調的是神經激素之重要性，例如腎素-血管收縮素-醛固酮系統。可惜的是藉由阻斷腎素-血管收縮素-醛固酮系統，糖尿病腎臟損傷或腎小球高過濾狀態並無法完全有效獲得緩解。因此，近來許多的臨床研究集中在腎小管因素對高過濾狀態之影響，例如鈉-葡萄糖共同轉運蛋白。腎小管因素是作用透過第2型鈉-葡萄糖共同轉運蛋白在腎臟近曲小管來增加對鈉離子的再吸收，藉由腎小管腎絲球回饋機制導致入球小動脈的擴張是造成其高過濾狀態的主要原因。臨床證據顯示第2型鈉-葡萄糖共同轉運蛋白抑制劑透過各種機轉不但能減少蛋白尿且能緩解蛋白尿的惡化。本篇綜論旨在詳細探討第2型鈉-葡萄糖共同轉運蛋白抑制劑在第二型糖尿病慢性腎衰竭病人治療中所扮演的角色。

Glomerular hyperfiltration predisposes nephron susceptible to damage irreversibly, thereby playing an important role in initiating the development of diabetic kidney disease. The pathogenesis of glomerular hyperfiltration in the past clinical trials has emphasized the importance of neurohormones such as the renin-angiotensin-aldosterone system (RAAS). Unfortunately, diabetic kidney damage or glomerular hyperfiltration does not completely get attenuated by RAAS blockade. Therefore, many recent clinical trials have focused on role of renal tubular factors to the hyperfiltration state such as the sodium-glucose cotransporter. The tubular factors are acting to increase sodium reabsorption in the renal proximal tubule through sodium-glucose Cotransporter-2 as the leading cause of hyperfiltration by afferent arteriole dilation via the tubuloglomerular feedback. Clinical evidence has suggested that sodium-glucose cotransporter-2 inhibitors (SGLT2i) can not only reduce development but attenuate deterioration of albuminuria through various mechanisms. This review aims to discuss the role of SGLT2i in type 2 diabetes patients with chronic kidney disease in detail.