Integrated management of IgA nephropathy: positioning disease-modifying and nephroprotective therapies across efficacy, access and acquisition cost

Résumé fourni par la source

IgA nephropathy (IgAN) is the most common primary glomerular disease worldwide and remains a major cause of chronic kidney disease (CKD) progression and kidney failure. Contemporary management has evolved from a predominantly supportive-care approach to a dual therapeutic paradigm that simultaneously addresses the immunological drivers of the disease and the consequences of chronic nephron loss. Nephroprotective options have expanded substantially. Sodium-glucose cotransporter-2 (SGLT2) inhibitors have demonstrated kidney and cardiovascular protection in broad CKD populations, with supportive evidence in IgAN. Endothelin receptor antagonism with sparsentan and atrasentan — and, more recently, non-steroidal mineralocorticoid receptor antagonism with finerenone — have also shown slowing of eGFR decline and reduction of albuminuria in IgAN. Disease-modifying therapy has progressed in parallel: targeted-release budesonide is currently the preferred option for patients with evidence of active immunological disease, with reduced-dose systemic glucocorticoids recommended where budesonide is unavailable or not reimbursed. Iptacopan, atacicept, telitacicept and sibeprenlimab represent the most immediate emerging therapeutic horizon, though regulatory approval remains pending in Europe for most of these agents. However, most pivotal trials were designed against a background of renin-angiotensin system (RAS) inhibition alone, which no longer fully reflects contemporary optimized conservative treatment. The key clinical question is therefore how to integrate these agents into a coherent, individualized, sequential treatment strategy, together with the appropriate duration of disease-modifying therapy. This narrative review proposes a phenotype-based, stepwise framework organized around three clinical scenarios: (1) isolated microscopic haematuria, which requires monitoring only; (2) stable kidney function with proteinuria and no evidence of immunological activity, managed with escalating nephroprotective therapy (RAS inhibition, SGLT2 inhibition, finerenone and sparsentan); and (3) progressive disease with markers of immunological activity, which requires disease-modifying therapies alongside the nephroprotective foundation; atypical presentations (rapidly progressive glomerulonephritis, pure nephrotic syndrome and thrombotic microangiopathy) are also briefly addressed. Particular attention is given to the positioning of emerging agents within the current regulatory and reimbursement landscape, drug acquisition costs, and the integration of cardiorenal protection into therapeutic decision-making.

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