Remission of Proteinuria in a Patient Affected by Crescentic IgA Nephropathy with Rapidly Progressive Glomerulonephritis Treated by Sodium-Glucose Cotransporter-2 Inhibitors: Casual or Causal Relationship?

• Published in: Kidney and dialysis 2022-12, Vol.2 (4), p.545-552
• Main Authors: De La Flor Merino, José C., Apaza Chávez, Jacqueline, Valga Amado, Francisco, Díaz Crespo, Francisco, Justo Avila, Pablo, Marschall, Alexander, Cieza Terrones, Michael, Núñez Ramos, Patricia, Ruiz Cicero, Elisa
• Format: Article
• Language: English
• Subjects: crescentic IgA nephropathy; rapidly progressive glomerulonephritis; sodium-glucose co-transporter-2 inhibitors
• ISSN: 2673-8236; 2673-8236
• DOI: 10.3390/kidneydial2040049

Crescentic IgA nephropathy (IgAN) with rapidly progressive glomerulonephritis (RPGN) is often associated with rapidly declining kidney function. Up to this date, specific therapy for crescentic IgAN is still unknown. Accumulating evidence suggests that sodium-glucose co-transporter-2 inhibitors (SGLT-2i) may have a role in standard therapy of glomerular diseases. However, it is unclear at what point in the natural history of specific glomerular diseases SGLT-2i can be beneficial. We report the clinical and histological features of a patient with crescentic IgAN that presented as an RPGN, who received intensive immunosuppression and renal replacement therapeutic (RRT). At the third month, the patient presented with significant improvement in his kidney function. At that point, we decided to start dapagliflozin in addition to his renin-angiotensin system (RAS) blocker, basing our decision on its proven renal benefits such as slowing the rate of decline in kidney function and reducing albuminuria. At the eighth month, the patient’s renal function gradually improved from serum Cr of 6.07 to 2.1 mg/dL; and urine albumin to creatinine ratio (UACR) declined from 5655 mg/g to 200 mg/g. The use of SGLT-2i in primary and secondary nondiabetic glomerular disease appears promising. It is crucial and necessary to accumulate more evidence for a more complete understanding of the mechanisms of the actions of SGLT-2i in non-diabetic glomerular disease.