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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
The sodium–glucose cotransporter 2 (SGLT2) is expressed in the brush border of proximal tubular cells and plays a key role in renal glucose reabsorption. SGLT2 inhibitors are widely used for the treatment of chronic kidney disease and heart failure due to their proven cardio-renal protective effects. However, information on SGLT2 protein expression in human kidneys remains limited. We report the first case of primary membranous nephropathy (MN) associated with a nearly complete loss of SGLT2 expression, accompanied by reversible glycosuria after treatment.
A 39-year-old man was admitted with renal failure and proteinuria. Laboratory findings showed renal failure with an elevated serum creatinine level of 5.6 mg/dL (estimated glomerular filtration rate: eGFR 10.3 mL/min/1.73 m²), hypoalbuminemia (2.2 g/dL), and marked glycosuria (0.47 g/dL) despite normal blood glucose and HbA1c (5.6%). Urinary β2-microglobulin (54,900 mg/L) and N-acetyl-β-D-glucosaminidase (18 U/L) levels were increased. A renal biopsy was performed for further evaluation, and renal tissue was examined using standard histological and immunohistochemical techniques. SGLT2 expression was examined by immunohistochemistry in approximately 200 renal biopsy samples obtained at our hospital, using highly specific anti-SGLT2 antibody validated by Sglt2-deficient rodents. Staining patterns were compared with a normal control kidney (28-year-old woman, thin basement membrane disease, eGFR 92.9 mL/min/1.73 m²) and a case of diabetic nephropathy (82-year-old man, eGFR 10 mL/min/1.73 m²).
Light microscopy revealed diffuse thickening of the glomerular basement membrane (GBM) with focal spike formation. Immunofluorescence showed granular deposits of IgG (++) and C3 (++), predominantly IgG4-positive, along the GBM. Electron microscopy demonstrated irregular GBM thickening with subepithelial electron-dense deposits, consistent with stage IV primary MN. Severe tubulointerstitial injury and chronic interstitial fibrosis were also observed.
Immunohistochemical staining revealed a complete loss of SGLT2 expression in the renal cortex, whereas control and diabetic nephropathy tissues showed preserved or reduced expression, respectively. Among 200 renal biopsy cases examined, this was the only case exhibiting a complete absence of SGLT2 staining.
Immunosuppressive therapy and an angiotensin II receptor blocker were initiated; however, remission of nephrotic syndrome was not achieved. One year after the treatment, urinary glucose became negative (0.03 g/dL). Subsequently, an SGLT2 inhibitor was introduced for renal protection, which led to an increase in urinary glucose excretion to 0.43 g/dL, suggesting recovery of SGLT2 function.
We report the first case of primary MN associated with loss of SGLT2 expression. The undetectable urinary glucose after therapeutic intervention for MN and the reappearance of glycosuria following SGLT2 inhibitor therapy suggest that SGLT2 expression may be reversible.
