IgA nephropathy (IgAN) is the most common cause of primary (idiopathic) glomerulonephritis in young people. Although slowly, it is known that end-stage renal disease occurs in 30% of patients within 20 years of presentation. It means that a 25 years old patient can require dialysis at age of 45.
The International IgA Prediction Tool can help to establish five-year risk of a 50% decline in eGFR, however it lacks risk factors such as hematuria and crescents. Supportive care without immunosuppressants is the main strategy recommended in IgAN, however one third of patients at risk of progression need to be identified and treated by more aggressive drugs.
In recent years, tailored based medicine is beginning to establish. These questions need to be answered in the coming years in order to improve management of IgAN and reduce the incidence of CKD and ESRD in young adults:
- Which biomarkers are in IgAN?
- What is the role of complement?
- What is the role of re-biopsy in refractory progressive IgAN?
- Will ACEi/ARB be used in normotensive IgAN with ematuria and/or low proteinuria (30-300 mg day)?
- Does combination therapy (ACEi plus ARB) improve renal outcome in IgAN?
- What about SGLT2i in IgAN?
- What is the impact of a low-antigen or gluten free diet?
- What about microbiota transplantation in IgA nephropathy?
- Can we use corticosteroids in IgAN with proteinuria >1 gram per day? Which is the best oral steroids regimen?
- Does TRF-budesonide deserve to be explored?
- Which immunosuppressive therapy in high risk IgAN (MMF, CYC, CNI, others)?
- What will be the place of biologics?
In recent years advances in renal histopathology and new treatments (immunomodulator, atacicept; complement inhibitors, avacopan, iptacopan, narsoplimab, cemdisiran, ravulizumab; endothelin A receptor, sparsentan and atrasentan; anti-APRIL BION -1301) are promisingly increasing.
This Research Topic is welcoming submissions of these main issues:
- IgAN: randomized clinical trials or evidence based medicine
IgA nephropathy (IgAN) is the most common cause of primary (idiopathic) glomerulonephritis in young people. Although slowly, it is known that end-stage renal disease occurs in 30% of patients within 20 years of presentation. It means that a 25 years old patient can require dialysis at age of 45.
The International IgA Prediction Tool can help to establish five-year risk of a 50% decline in eGFR, however it lacks risk factors such as hematuria and crescents. Supportive care without immunosuppressants is the main strategy recommended in IgAN, however one third of patients at risk of progression need to be identified and treated by more aggressive drugs.
In recent years, tailored based medicine is beginning to establish. These questions need to be answered in the coming years in order to improve management of IgAN and reduce the incidence of CKD and ESRD in young adults:
- Which biomarkers are in IgAN?
- What is the role of complement?
- What is the role of re-biopsy in refractory progressive IgAN?
- Will ACEi/ARB be used in normotensive IgAN with ematuria and/or low proteinuria (30-300 mg day)?
- Does combination therapy (ACEi plus ARB) improve renal outcome in IgAN?
- What about SGLT2i in IgAN?
- What is the impact of a low-antigen or gluten free diet?
- What about microbiota transplantation in IgA nephropathy?
- Can we use corticosteroids in IgAN with proteinuria >1 gram per day? Which is the best oral steroids regimen?
- Does TRF-budesonide deserve to be explored?
- Which immunosuppressive therapy in high risk IgAN (MMF, CYC, CNI, others)?
- What will be the place of biologics?
In recent years advances in renal histopathology and new treatments (immunomodulator, atacicept; complement inhibitors, avacopan, iptacopan, narsoplimab, cemdisiran, ravulizumab; endothelin A receptor, sparsentan and atrasentan; anti-APRIL BION -1301) are promisingly increasing.
This Research Topic is welcoming submissions of these main issues:
- IgAN: randomized clinical trials or evidence based medicine
