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Introduction

IgA nephropathy is the most frequent glomerular disease worldwide. Its clinical course is variable, but in most cases there is a decline in renal function and, despite advances in our understanding of its pathogenesis, treatment strategies haven’t changed much over the last 2 or 3 decades. Patients at greatest risk of progressive renal impairment are those with hypertension, proteinuria >1 g/24 h and reduced glomerular filtration rate at diagnosis [1].

There are no disease-specific therapies for IgA nephropathy and the established treatment approach for most patients is to apply supportive measures that include the use of renin-angiotensin-aldosterone system blockade (RAAS) [1, 2] and more recently SGLT2i (as evidenced by the DAPA-CKD study [3] and by the subanalysis of EMPAKIDNEY study, in which 25% of patients were affected by glomerular diseases) [4].

At present, there is insufficient evidence for the additional use of immunosuppressive agents, antiplatelet agents or anticoagulants. The role of immunosuppressive therapy remains controversial and is usually reserved for patients who don’t respond to supportive measures [2]. 

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