Navigating Novel Pathways and Treatment Decisions in IgA Nephropathy - Episode 2
Guidelines now call for treating the immune driver of disease and providing supportive care at the same time. The panel considers how ambitious targets have become realistic, and why access still limits what clinicians can offer.
Dr. Wadhwani asks Dr. Geara whether optimized supportive care can be sufficient. Dr. Geara explains that earlier guidelines treated supportive care first and added IgA-directed therapy later, but current guidelines recommend addressing both at the same time. Supportive care remains important, and its umbrella keeps growing. Still, he stresses that IgAN is an inflammatory disease, so few patients should rely on supportive care alone. Only a patient with well-documented stability over several years might qualify.
Dr. Cheung agrees that most patients benefit from added targeted therapy, with supportive care continued in the background, because these classes have shown better eGFR preservation. Dr. Cheung and Dr. Wadhwani highlight residual proteinuria as a concern for both renal and cardiovascular risk. Dr. Cheung says the KDIGO targets once seemed unrealistic but now look well within reach. The approach is to start effective therapy early, monitor frequently, and switch when response is insufficient. Dr. Wadhwani adds that data shown at Kidney Week suggest even the eGFR target is achievable.
On real-world challenges, Dr. Geara describes six approved therapies in the United States but uneven access, since most require insurance approval and are expensive. He adds that proteinuria and eGFR have shortcomings for assessing activity and response, and neither tells clinicians which drug to give or for how long. Dr. Wadhwani notes that no approved agent was compared head to head, populations differed, and baseline SGLT2 inhibitor use varied. Approval does not guarantee access.
Up next, in "IgAN Pathogenesis: How Each Drug Class Targets the Multi-Hit Pathway," Dr. Cheung maps each therapeutic class onto the points in the pathway where IgAN disease activity arises.