Case Study: Inhibitors of the sodium-glucose cotransporter 2 (SGLT2) are a new class of antihyperglycemic drugs with hypoglycemic effect, that act by inhibiting glucose reabsorption in the proximal tubule of the glomerulus, with cardiovascular and renal pleiotropic effects. Clinical studies have shown glucose-dependent and independent mechanisms underlying the renoprotective effects of this inhibition. We present the case of a 55-year-old man with CKD secondary to IgA nephropathy (IgAN), hypertension, dyslipidemia and hyperuricemia. It was referred to nephrology consultation in 2010 due to CKD and nephrotic proteinuria. Laboratorial workup showed: serum creatinine 1.5mg/dL, proteinuria 3800mg/day; mild erythrocyturia and elevated immunoglobulin A. He underwent renal biopsy with a diagnosis of IgAN with mild chronicity. He presented proteinuria remission up to 150mg/day under dual blockade of the renin-angiotensin-aldosterone system. Since 2015, only under antagonist receptors of the angiotensin (ARA) II at maximum dose, proteinuria remained under 1800mg/day. In 2018, a non-dihydropyridine calcium channel antagonist was added, maintaining a gradual worsening of proteinuria (2900mg/day). In early 2021 proteinuria worsened to 4754mg/day, without nephrotic syndrome. A repeat renal biopsy was considered and the off-label use of iSGLT-2 in non-diabetic proteinuria was discussed with the patient. With informed consent, dapagliflozin (10 mg, id) was started and, after 3 months, a reduction to 1000mg/day of proteinuria was observed. Presently he presents 800 mg/day and renal biopsy was postponed. This case describes a significant reduction in proteinuria in a non-diabetic patient with IgAN after the introduction of iSGLT-2. This therapeutic change additionally translated into weight loss and improved blood pressure control. The reduction in glomerular hyperfiltration and plasma glucose by iSGLT-2 has been associated with a decrease in proteinuria and tubulointerstitial inflammation. Additionally, it is known that podocytes may express the SGLT-2 transporter, which may explain the benefits of using these drugs in proteinuric kidney disease.