Canagliflozin Markedly Decreased Proteinuria in a Patient With IgA Nephropathy

Abstract

IgA nephropathy (IgAN) remains one of the most common forms of glomerulonephritis, especially in developed countries with a low prevalence of infectious diseases. Despite supportive measures that slow the rate of progression of chronic kidney disease (CKD) in IgAN, many patients still progress to end-stage kidney disease. Proteinuria has been shown to be an adverse prognostic factor in IgAN. Data support the use of proteinuria reduction as a reasonably likely surrogate endpoint for a treatment's effect on progression to end-stage renal disease (ESRD) in IgAN. Currently employed immunosuppressive strategies lack conclusive efficacy data, while there is evidence for treatment-induced toxicity. The current standard of care for the management of IgAN is intensive goal-directed supportive care. Recently the role of sodium-glucose cotransporter 2 (SGLT2) inhibitors in decreasing proteinuria and progression of CKD is widely being recognized. In this case report, we present a 44-year-old male with proteinuria and biopsy-proven IgAN who remained in remission after six months of steroids using the Pozzi protocol. He developed proteinuria five years after remission. At this point, canagliflozin was added to his angiotensin-receptor blocker (ARB) therapy resulting in a significant reduction in his proteinuria. Our case report may intrigue researchers to look into the role of canagliflozin in decreasing albuminuria in non-diabetic kidney disease, thus slowing the progression to ESRD.