<p>Earlier recognition of anti-neutrophil cytoplasmic antibody-associated vasculitis has led to more timely treatment initiation and improvements in patient survival, despite limited available therapeutic options. Current drugs can induce remission in most patients, but therapies are not individualized, with consequent over-treatment of some patients and under-treatment of others, leading to considerable morbidity from both disease and therapy. Diverse research strategies, from large clinical datasets to single-cell molecular analyses, have improved understanding of antibody-associated vasculitis biology substantially, with implications for patient management. Longitudinal data from registries and trial databases have highlighted variations in the patterns and progression of kidney disease. Efforts to improve current biological readouts of disease activity have tried to identify more dynamic and clinically applicable biomarkers to inform, in real time, the level of therapy required. Examples of such readouts include urinary levels of CD163 and CC-chemokine ligand 2, urinary T cell numbers and serum levels of various immune biomarkers, although further validation studies are required. Several important questions — how to prevent kidney disease progression, predict relapse and determine immunological quiescence to inform duration of therapy — remain incompletely answered. Here, we highlight some of the latest research advances that can help to inform clinicians about the biology of disease and might ultimately enable customization of treatment.</p>