IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide and a major cause of progressive chronic kidney disease. Systemic corticosteroids are commonly used in high-risk patients but are frequently limited by inadequate response and significant adverse effects. We present the case of a 46-year-old woman with biopsy-confirmed IgAN who developed persistent microscopic hematuria and nephritic-range proteinuria. After six months of treatment with high-dose systemic prednisone, renin-angiotensin-aldosterone system blockade, and a sodium-glucose cotransporter-2 inhibitor, there was no clinical improvement, and she experienced marked cushingoid toxicity. Due to treatment failure and intolerance to systemic glucocorticoids, targeted-release budesonide was initiated. Over six months, proteinuria decreased from 2,536 mg/day to 66 mg/day, hematuria completely resolved, and estimated glomerular filtration rate improved from 65 to 80 mL/min/1.73 m². The treatment was well tolerated without recurrence of systemic steroid-related adverse effects. This case highlights targeted-release budesonide as an effective therapeutic option for selected patients with IgAN who fail or cannot tolerate systemic corticosteroid therapy.
Manrique-Pizarro et al. (2026) studied this question.