An update on the treatment of IgA nephropathy

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Purpose of review

The treatment of IgA nephropathy (IgAN) has been limited by several controversies in the literature, including the benefits of corticosteroids in addition to optimized renin–angiotensin system blockers (RASBs), in those with lower estimated glomerular filtration rate (eGFR), or in different ethnic groups. Recent studies have attempted to address these issues.

Recent findings

Two observational studies suggest the efficacy of corticosteroids in those with lower eGFR, but with a higher risk of adverse events. The Supportive versus Immunosuppressive Therapy for the Treatment of Progressive IgA Nephropathy (STOP-IgAN) trial compared immunosuppression with supportive care in addition to optimized RASB, and suggests that corticosteroids (but not cyclophosphamide/azathioprine) may reduce proteinuria but the effect on renal function is not clear, that immunosuppression is associated with a high risk of adverse events and that optimal RASB is very effective at lowering proteinuria and the short-term risk of renal function decline. The Therapeutic Evaluation of Steriods in IgA Nephropathy Global (TESTING) trial compared corticosteroids with placebo in addition to optimized RASB, and demonstrated a decreased risk of renal function decline and lower proteinuria, but a higher risk of adverse events. Additional trials demonstrate the potential efficacy of enteric-budesonide but not rituximab on proteinuria reduction, and conflicting findings with mycophenolate mofetil.


Until less toxic therapies for IgAN are available, treatment with corticosteroids will need to be made in the context of conflicting evidence, and should likely be limited to patients at highest risk of disease progression who understand the significant risk of adverse events.

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