Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a small vessel vasculitis according to the 2012 revised Chapel Hill Consensus Conference Nomenclature of Vasculitides, most frequently presenting as microscopic polyangiitis (MPA) or granulomatosis with polyangiitis (GPA) [
1,
2]. Renal involvement is a common and severe complication of AAV potentially resulting in pauci-immune necrotizing and crescentic ANCA glomerulonephritis (GN) with acute kidney injury (AKI), end-stage renal disease (ESRD) or death [
2]. Clinicopathologic studies of the European Vasculitis Study Group (EUVAS) demonstrated that distinct glomerular lesions are related to renal outcome in ANCA GN [
3‐
6]. Derived from these studies, histopathological subgrouping into four classes (focal, crescentic, mixed, and sclerotic) as defined by Berden et al. was shown to predict long-term renal survival rates [
7]. However, multivariable analyses demonstrated no improvement in outcome prediction in most of these studies, mainly attributed to no outcome difference in the crescentic and mixed classes [
8‐
16]. Therefore, Brix et al. suggested the ANCA renal risk score (ARRS) by incorporating tubular atrophy/interstitial fibrosis (TA/IF) to the percentage of normal glomeruli and baseline glomerular filtration rate (GFR) to predict ESRD in patients with AAV, underscoring a pathomechanistic link between tubulointerstitial and glomerular lesions in ANCA GN [
17]. Bowman’s capsule rupture was first described more than 30 years ago and we recently described that Bowman’s capsule rupture links glomerular damage to tubulointerstitial inflammation in ANCA-associated glomerulonephritis in a considerable subset of patients with ANCA GN [
18]. An increased fraction of glomeruli affected by extensive Bowman’s capsule rupture in ANCA GN was associated with tubulointerstitial inflammation, suggesting that interstitial inflammation may also have predictive value in assessing the risk of decline in kidney function in ANCA GN [
4,
10,
19]. Furthermore, we and others have previously described that focal Bowman’s capsule rupture with less extensive lesions was observed even more frequently in ANCA GN [
20,
21]. The concept that tubulointerstitial injury mediates impairment of renal function was described more than five decades ago, in studies showing that decline of kidney function exhibited a stronger correlation with the severity of tubulointerstitial rather than with glomerular damage [
22]. We recently characterized intrarenal subtypes of immune cell infiltrates in myeloperoxidase (MPO)-ANCA versus proteinase 3 (PR3)-ANCA GN, associated with distinct glomerular and tubulointerstitial lesions [
23]. However, the association between Bowman’s capsule rupture and distinct immune cell subtypes has not been explored so far. Therefore, herein we provide comprehensive histological subtyping of immune cell infiltrates in association with extensive or focal Bowman’s capsule rupture in a cohort of 44 patients with ANCA GN confirmed by renal biopsy. The cohort comprises cases who underwent a kidney biopsy between 2015 and 2020 in a single-center, and this study represents a further step in the description of the relationship between Bowman’s capsule rupture and kidney damage [
18].