The Role and Mechanism of SGLT2 Inhibitors in Chronic Kidney Disease

Chronic kidney disease (CKD) refers to structural or functional abnormalities of the kidneys caused by various factors lasting ≥3 months, or a decline in glomerular filtration rate (GFR) of <60 mL/min of unknown cause lasting ≥3 months. Its primary causes include diabetic kidney disease, hypertensive nephropathy, IgA nephropathy, membranous nephropathy, and lupus nephritis, among others. As a new class of antidiabetic drugs, sodium-glucose cotransporter 2 inhibitors (SGLT2i) have been shown in numerous clinical studies and animal experiments to be effective in treating CKD of various etiologies. The renoprotective effects of SGLT2 inhibitors are independent of their glucose-lowering effects. Through mechanisms such as hemodynamics, oxidative stress, and anti-fibrosis, they reduce serum creatinine and urinary protein levels, thereby slowing the progression of CKD. This review primarily summarizes clinical and basic research on SGLT2i in the treatment of CKD and analyzes the signaling pathways through which SGLT2i exerts its effects on CKD. This demonstrates that SGLT2 inhibitors can delay the progression of kidney function decline and improve outcomes in patients across various subtypes through multiple mechanisms. They are suitable for patients with CKD of different etiologies and across different estimated glomerular filtration rate (eGFR) categories, indicating the significant potential and promising prospects for the widespread use of SGLT2 inhibitors in patients with CKD.