ArticleKidney international reports2026
Immune Profiling Identifies High-Risk Neutrophil-Rich Subtype in Checkpoint Inhibitor Nephritis.
Article in Kidney international reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Response to the Letter to the Editor Entitled "Beyond Lymphocytic Inflammation: Immune Architecture as a Determinant of Renal Outcomes".Kidney international reports · 2026Article
- Beyond Lymphocytic Inflammation: Immune Architecture as a Determinant of Renal Outcomes.Kidney international reports · 2026Article
- Linoleoyl-lysophosphatidylcholine drives non-inflammatory apoptosis in neutrophils via lipid rafts.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
30 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Immune checkpoint inhibitor (ICI)-induced acute interstitial nephritis (AIN) (ICI-AIN) is the leading cause of ICI-associated acute kidney injury (AKI). ICI-AIN is characterized by mononuclear immune infiltrates, although the mechanisms behind their toxicity remain unclear. We aimed to characterize these infiltrates in kidney biopsies and assess their correlation with clinical outcomes and therapeutic responses. Methods: We retrospectively analyzed 49 biopsy-proven ICI-AIN cases using multiplex immunofluorescence to quantify immune cells (macrophages, neutrophils, B cells, T cells, and plasmocytes). Unsupervised clustering was used to identify patient groups, which we then correlated with clinical presentation and outcomes. Finally, we explored the role of C5a/C5aR1 in neutrophil recruitment. Results: Unsupervised clustering revealed 3 immune phenotypes as follows: (i) low mononuclear (cluster 1), (ii) high mononuclear (cluster 2), and (iii) neutrophil-rich (cluster 3). Cluster 3 was associated with higher systemic inflammation (C-reactive protein: 84 vs. 15-24 mg/l, Conclusion: Our findings identify distinct ICI-AIN subtypes, with a neutrophil-rich cluster linked to complement activation and poor prognosis, offering insights into refining diagnosis and treatment strategies.
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