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Rapid Remission of Steroid-Refractory IgA Nephropathy With Targeted-Release Budesonide: A Case Report
Paola A Manrique-Pizarro1, Emmanuel Cordero2
1Internal Medicine, Universidad Autónoma de Guadalajara, Trujillo Alto, PRI.
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.
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.
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