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IgA nephropathy (Berger's disease) — how IgA deposits damage the kidneys, the blood-in-urine pattern, diagnosis by biopsy, and modern treatment including SGLT2 inhibitors and budesonide.
Evidence reviewed & updated: 2026-08 — reflects the latest published trials and guidelines.
IgA nephropathy is the most common primary glomerulonephritis worldwide — IgA antibody deposits lodge in the kidney's filter, causing blood and protein in urine, and slowly damaging it. It often follows respiratory or GI infections (the classic 'synpharyngitic hematuria'). Up to 30-40% progress to kidney failure over decades — but modern therapy (SGLT2i, optimized RAAS blockade, targeted treatments like budesonide) has improved the outlook.
IgA nephropathy (Berger's disease) occurs when abnormal IgA immune complexes deposit in the glomeruli (the kidney's filters). The deposits trigger inflammation — blood and protein leak into urine, and over years, scarring (glomerulosclerosis) accumulates.
It commonly shows up as visible blood in the urine 1-2 days after a respiratory or GI infection — the 'synpharyngitic hematuria' pattern that distinguishes it from post-streptococcal nephritis (which comes weeks after). Many cases are silent, found on routine urinalysis.
Diagnosis is by kidney biopsy showing dominant IgA deposits in the mesangium. Workup includes urine protein (UACR), eGFR, BP, and excluding other causes (lupus, IgA vasculitis, liver disease).
The risk of progression is driven by: proteinuria (especially >1 g/day), hypertension, reduced eGFR at diagnosis, and certain biopsy findings (crescents). These markers define who needs aggressive therapy.
The foundation for anyone with proteinuria: ACEi/ARB (renin-angiotensin blockade) plus SGLT2 inhibitors — the same kidney-protective stack as diabetic CKD, now proven in IgA (DAPA-CKD and EMPA-KIDNEY included IgA patients).
For high-risk patients (proteinuria >1 g/day despite optimization): a 6-month steroid course, or budesonide (Nefecon) — the targeted-release gut steroid shown in the NefIgArd trial to reduce proteinuria and preserve eGFR. Rapidly progressive disease with crescents needs more intensive immunosuppression (cyclophosphamide/rituximab per protocol).
In advanced CKD, standard renal diet and monitoring rules apply; transplant is a good option (disease recurs in grafts but graft loss is uncommon).
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