IgA Nephropathy: What Is New in Treatment Options?
IgA nephropathy (IgAN), first described in 1968, is one of the most common forms of glomerulonephritis and can progress to end-stage kidney disease (ESKD) in 25 to 30 percent of patients within 20 to 25 years from the onset. It is histologically characterized by mesangial proliferation with prominen...
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2024-12-01
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| Series: | Kidney and Dialysis |
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| author | Roberto Scarpioni Teresa Valsania |
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| description | IgA nephropathy (IgAN), first described in 1968, is one of the most common forms of glomerulonephritis and can progress to end-stage kidney disease (ESKD) in 25 to 30 percent of patients within 20 to 25 years from the onset. It is histologically characterized by mesangial proliferation with prominent IgA deposition. The prognosis may be difficult to predict, but important risk factors for disease progression of kidney disease have been recognized: usually proteinuria above 0.75–1 g/day with or without hematuria, hypertension, high-risk histologic features (such as crescent formation, immune deposits in the capillary loops, mesangial deposits, glomerulosclerosis, tubular atrophy, interstitial fibrosis, and vascular disease), and a reduced Glomerular Filtration Rate (GFR). In the absence of reliable specific biomarkers, current standards of care are addressed to decrease proteinuria, as a surrogate endpoint, and control blood pressure. For a long time, corticosteroids have been considered the only cure for proteinuric patients or those at risk of progression to ESKF; however, unfortunately, like other immunosuppressive agents, they are burdened with high collateral risks. Therefore, optimal treatment remains a challenge, even if, to date, clinicians have many more options available. Here, we will review the main therapies proposed, such as the stronghold of RAAS inhibition and the use of SGLT2 inhibitors; it is expected that ongoing clinical trials may find other therapies, apart from corticosteroids, that may help improve treatment, including both immunosuppressive monoclonal antibodies and other strategies. At the current time, there are no disease-specific therapies available for IgAN, because no largescale RCTs have demonstrated a reduction in mortality or in major adverse kidney or cardiovascular events with any therapy. |
| format | Article |
| id | doaj-art-2437bd78e5ff412cb1fb81215b2d03cf |
| institution | OA Journals |
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| language | English |
| publishDate | 2024-12-01 |
| publisher | MDPI AG |
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| series | Kidney and Dialysis |
| spelling | doaj-art-2437bd78e5ff412cb1fb81215b2d03cf2025-08-20T02:00:23ZengMDPI AGKidney and Dialysis2673-82362024-12-014422324510.3390/kidneydial4040019IgA Nephropathy: What Is New in Treatment Options?Roberto Scarpioni0Teresa Valsania1Unit of Nephrology and Dialysis, Department of Medicine, AUSL Hospital “Guglielmo da Saliceto”, via Taverna 49, 29121 Piacenza, ItalyUnit of Nephrology and Dialysis, Department of Medicine, AUSL Hospital “Guglielmo da Saliceto”, via Taverna 49, 29121 Piacenza, ItalyIgA nephropathy (IgAN), first described in 1968, is one of the most common forms of glomerulonephritis and can progress to end-stage kidney disease (ESKD) in 25 to 30 percent of patients within 20 to 25 years from the onset. It is histologically characterized by mesangial proliferation with prominent IgA deposition. The prognosis may be difficult to predict, but important risk factors for disease progression of kidney disease have been recognized: usually proteinuria above 0.75–1 g/day with or without hematuria, hypertension, high-risk histologic features (such as crescent formation, immune deposits in the capillary loops, mesangial deposits, glomerulosclerosis, tubular atrophy, interstitial fibrosis, and vascular disease), and a reduced Glomerular Filtration Rate (GFR). In the absence of reliable specific biomarkers, current standards of care are addressed to decrease proteinuria, as a surrogate endpoint, and control blood pressure. For a long time, corticosteroids have been considered the only cure for proteinuric patients or those at risk of progression to ESKF; however, unfortunately, like other immunosuppressive agents, they are burdened with high collateral risks. Therefore, optimal treatment remains a challenge, even if, to date, clinicians have many more options available. Here, we will review the main therapies proposed, such as the stronghold of RAAS inhibition and the use of SGLT2 inhibitors; it is expected that ongoing clinical trials may find other therapies, apart from corticosteroids, that may help improve treatment, including both immunosuppressive monoclonal antibodies and other strategies. At the current time, there are no disease-specific therapies available for IgAN, because no largescale RCTs have demonstrated a reduction in mortality or in major adverse kidney or cardiovascular events with any therapy.https://www.mdpi.com/2673-8236/4/4/19IgA nephropathyBerger diseaseglomerulonephritisproteinuriatreatmentchronic kidney disease |
| spellingShingle | Roberto Scarpioni Teresa Valsania IgA Nephropathy: What Is New in Treatment Options? Kidney and Dialysis IgA nephropathy Berger disease glomerulonephritis proteinuria treatment chronic kidney disease |
| title | IgA Nephropathy: What Is New in Treatment Options? |
| title_full | IgA Nephropathy: What Is New in Treatment Options? |
| title_fullStr | IgA Nephropathy: What Is New in Treatment Options? |
| title_full_unstemmed | IgA Nephropathy: What Is New in Treatment Options? |
| title_short | IgA Nephropathy: What Is New in Treatment Options? |
| title_sort | iga nephropathy what is new in treatment options |
| topic | IgA nephropathy Berger disease glomerulonephritis proteinuria treatment chronic kidney disease |
| url | https://www.mdpi.com/2673-8236/4/4/19 |
| work_keys_str_mv | AT robertoscarpioni iganephropathywhatisnewintreatmentoptions AT teresavalsania iganephropathywhatisnewintreatmentoptions |