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Scoping review finds SGLT2 inhibitors show kidney protection in IgA nephropathy

Scoping review finds SGLT2 inhibitors show kidney protection in IgA nephropathy
Photo by Navy Medicine / Unsplash
Key Takeaway
Consider SGLT2 inhibitors for kidney protection in IgA nephropathy, but note limited disease-specific trial data.

This scoping review summarizes the current evidence on SGLT2 inhibitors for patients with IgA nephropathy (IgAN). The authors reviewed randomized, observational, and mechanistic studies to evaluate kidney outcomes, proteinuria, and mortality.

Key findings include that two large randomized controlled trials (DAPA-CKD and EMPA-KIDNEY) provided randomized evidence supporting kidney-protective effects in IgAN subgroups. Complementary observational and real-world studies consistently demonstrated clinically meaningful reductions in proteinuria and stabilization of kidney function trajectories. Mortality data specific to IgAN remain limited, though indirect evidence from broader CKD populations suggests biological plausibility for cardiovascular and survival benefits.

The review notes important limitations: disease-specific randomized trials remain limited, and mortality data specific to IgAN are lacking. No pooled effect sizes or safety data are reported.

For clinicians, the consistent signals from randomized, observational, and mechanistic evidence support the role of SGLT2 inhibitors as kidney-protective therapy in IgAN, but caution is warranted given the absence of dedicated IgAN trials and limited mortality data.

Study Details

Study typeRct
EvidenceLevel 2
PublishedApr 2026
View Original Abstract ↓
To conduct a scoping review mapping the extent, nature, and consistency of available evidence regarding the effects of sodium–glucose cotransporter-2 (SGLT2) inhibitors on kidney function, proteinuria, kidney outcomes, and mortality in patients with IgA nephropathy (IgAN). This scoping review was conducted in accordance with the PRISMA-ScR guidance. Randomized controlled trials (RCTs) including patients with IgAN were identified to characterize high-level efficacy signals. Observational studies, real-world cohorts, and mechanistic investigations were additionally included to contextualize and extend the randomized evidence. Findings were mapped across five predefined outcome domains: acute eGFR dip, chronic eGFR slope, proteinuria reduction, kidney outcomes, and mortality. Two large randomized controlled trials, DAPA-CKD and EMPA-KIDNEY, provided randomized evidence supporting kidney-protective effects of SGLT2 inhibitors in IgAN subgroups. Complementary observational and real-world studies consistently demonstrated clinically meaningful reductions in proteinuria, stabilization of kidney function trajectories, and mechanistic patterns linking early hemodynamic responses with longer-term renal benefit. Mortality data specific to IgAN remain limited; however, indirect evidence from broader CKD populations suggests biological plausibility for cardiovascular and survival benefits. The available evidence supporting SGLT2 inhibitors in IgA nephropathy is broad, convergent across study designs, and mechanistically coherent. Although disease-specific randomized trials remain limited, consistent signals from randomized, observational, and mechanistic evidence support the role of SGLT2 inhibitors as kidney-protective therapy in IgAN and highlight priorities for future IgAN-focused research. https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=630522, identifier (CRD42025630522).
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