Abstract
IgA nephropathy is an inflammatory renal disease characterised by the deposition of IgA in the glomerular mesangium and is the most commonly reported primary glomerulonephritis worldwide. Thirty to forty percent of patients with the disease develop progressive renal function decline, requiring renal replacement therapy within two decades of diagnosis. Despite this, accurate individual risk stratification at diagnosis and predicting treatment response remains a challenge. Furthermore, there are currently no disease specific treatments currently licensed to treat the condition due to long standing challenges in the nature and prevalence of the disease. Despite this, there have been exciting recent advances in the field that may represent paradigm shifts in the way IgA nephropathy is managed in the near future. In this review, we explore the evidence base informing current approaches to management and explore new strategies and future directions in the diagnosis and management of IgA nephropathy.
Highlights
IgA nephropathy (IgAN) is an inflammatory renal disease characterised by the deposition of IgA in the glomerular mesangium [1]
The TESTING trial, which recruited the majority of patients from China, compared methylprednisolone (0.8 mg/ kg/day; maximum 48 mg/day) against placebo, and demonstrated that a relatively high corticosteroid dose had potential renal benefit, with a reduction of patients in the methylprednisolone group reaching the primary composite renal outcome (40% decrease in estimated glomerular filtration rate (eGFR), endstage renal disease (ESRD) or death due to kidney failure; 5.9% vs 15.9% in the placebo group), and a reduced mean annual eGFR decline in this group (− 1.79 in the methylprednisolone group vs − 6.95 ml/min/1.73 m2 in the placebo group)
Fostamatinib is a selective Spleen tyrosine kinase (SYK) inhibitor that has been studied in rheumatoid arthritis (RA) where it lowered disease activity compared to placebo
Summary
IgA nephropathy (IgAN) is an inflammatory renal disease characterised by the deposition of IgA in the glomerular mesangium [1]. The TESTING trial, which recruited the majority of patients from China, compared methylprednisolone (0.8 mg/ kg/day; maximum 48 mg/day) against placebo, and demonstrated that a relatively high corticosteroid dose had potential renal benefit, with a reduction of patients in the methylprednisolone group reaching the primary composite renal outcome (40% decrease in eGFR, ESRD or death due to kidney failure; 5.9% vs 15.9% in the placebo group), and a reduced mean annual eGFR decline in this group (− 1.79 in the methylprednisolone group vs − 6.95 ml/min/1.73 m2 in the placebo group) This came at a cost with a significantly increased rate of adverse events, and the study was terminated early by the data safety monitoring committee due to the increased number of life-threatening infections in the treatment arm [65]. It is again hoped that should any of the drugs currently being evaluated prove to be efficacious and safe in IgAN that there will be a drive to test them in IgA vasculitis
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