IgA Nephropathy is a kidney disorder characterized by inflammation of the glomeruli, which are the kidneys’ filtering units. IgAN can lead to blood and protein in the urine, high blood pressure, and progressive loss of kidney function. It could be the first disease with significant prevalence to be treated with therapies targeting the complement system.1 The need is great for patients with this condition, as treatment has historically focused on supportive treatments addressing hypertension and proteinuria (protein in the urine), and most patients with higher residual proteinuria still progress to kidney failure, which is up to half of patients within 20 years of clinical presentation.2-3 Kidney disease progression in IgAN is caused by the formation and deposition of immune complexes composed of galactose-deficient IgA1 (Gd-IgA1) and Gd-IgA1 autoantibodies (anti-Gd-IgA1 antibodies) in the glomeruli, where they trigger complement-mediated inflammation that can lead to kidney function loss.2
A definitive diagnosis of IgAN requires a kidney biopsy. Special preparations with immunofluorescence or immunoperoxidase staining demonstrating the presence of dominant or co-dominant deposition of IgA help in this process.4 Because of a broad range of presentations spanning from gross hematuria to microscopic hematuria, nephrotic syndrome and acute kidney injury, diagnosis can often be delayed. Healthcare professionals (HCPs) need to better able to identify patients at high risk of developing end-stage kidney disease so that they can guide more optional treatment decisions and implement interventions at an earlier stage and prevent/halt the disease progression. Targeting complement activation could lead to important new treatments for IgAN, which is the most common glomerulonephritis worldwide.3
Current treatment approaches for IgA nephropathy primarily focus on blood pressure control, reducing proteinuria, and immunosuppression in selected cases. There is significant gap in the understanding of key mechanistic pathways of effective and targeted emerging therapies (eg, factor B, endothelin receptors and APRIL/BAFF), usage of renal biopsy scoring systems for prognosis prediction, and of clinical protocols for treating IgAN. Recent clinical developments are shifting treatment paradigms as a variety of new and emerging therapeutics with different mechanisms of action and/or targeted forms of delivery are becoming available. Given the rapidly evolving therapeutic landscape, it can be challenging for clinicians to stay up to date with the latest clinical evidence on new and emerging therapies, including their mechanism of action, efficacy and safety data, and their potential impact on IgAN disease progression. Innovative, engaging educational activities are needed to deliver the essential scientific evidence and latest updates.