Immunoglobulin A nephropathy (IgAN) remains the leading primary glomerular disease worldwide, with a majority of patients reaching kidney failure within their lifetimes. IgAN is a heterogeneous glomerular disorder characterized by mesangial deposition of galactose-deficient immunoglobulin A1 containing immune complexes that induce glomerular injury and nephron loss. The primary therapeutic goal in treating IgAN is reduction of nephron loss from the time of diagnosis. Management ideally incorporates interventions targeting both immunologic and nonspecific chronic kidney disease pathomechanisms. Multitargeted approaches that simultaneously target the production of pathogenic immunoglobulin A immune complexes, address the consequences of ongoing nephron loss, halt glomerular inflammation, and inhibit profibrotic signals in the glomerulus and tubulointerstitium will provide maximal benefit. Given significant advances in the understanding of disease pathogenesis and the acceptance of surrogate outcomes (including proteinuria reduction) for accelerated drug approval, there has been a plethora of pharmacological agents recently evaluated and approved to treat IgAN. This review highlights the latest therapeutic developments in the field.
Rajasekaran et al. (Tue,) studied this question.