Reposted by Sarah Sanghavi
Sarah Sanghavi
@sarahsanghavi.bsky.social
1.3K followers 525 following 181 posts
Intensivist, Nephrologist @uwnephrology.bsky.social | Via UT Austin, UTSW, WashU, and Mt. Sinai | Views mine nephrology.uw.edu/people/faculty/sa… #nephsky #medsky
![Figure 1 Therapeutic targets and positioning of treatments in IgA nephropathy (IgAN). Reflecting our latest understanding, treatments should target IgAN-specific drivers for nephron loss (Hits 1-3, Hit 4) and generic response to IgAN-induced nephron loss. Drugs targeting the IgAN-specific drivers for nephron loss likely act on different mechanisms of the 4-hit hypothesis. Triangles denote that a drug class most likely exerts its key actions on either Hits 1-3 or Hit 4 but may target all hits to a variable extent as indicated by their lengths of the triangle. Nefecon, APRIL inhibitors, and dual APRIL-BAFF inhibitors are shown as having a predominant effect on the production of pathogenic forms of IgA and IgA containing immune complexes (IgA-ICs) [Hits 1-3] while systemic glucocorticoids and complement inhibitors are shown as having a predominant anti-inflammatory effect on IgA-IC mediated kidney injury [Hit 4]. Interventions to manage the generic response to IgAN-induced nephron loss include lifestyle modifications, RASi or DEARA use with or without SGLT2i, or use of a DEARA or a combination of ERA and RASi. Additional strategies may also include the use of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors in select patients. The drugs listed here do not imply a recommended ranking or delivery sequence. APRIL, a proliferation-inducing ligand; BAFF, B cell–activating factor; DEARA, dual endothelin angiotensin receptor antagonist; ERA, endothelin type A receptor antagonist; RASi, renin-angiotensin system inhibitor; SGLT2i, sodium-glucose cotransporter-2 inhibitor.](https://cdn.bsky.app/img/feed_thumbnail/plain/did:plc:33h4q6nw674jdcwfxaq2m2nl/bafkreidryzyepbhcxh4g7cjglwmmk6tfgyxmujh55el3ey76ki4zp4qa5i)
