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Related Concept Videos

Immunodeficiency Diseases01:25

Immunodeficiency Diseases

Immunodeficiency disorders are conditions in which the immune system's ability to fight infectious disease and cancer is compromised or entirely absent. The immune system comprises a complex network of cells, tissues, and organs that work together to protect the body from potentially harmful invaders. When this system is deficient or not functioning properly, it leaves the body susceptible to infections, diseases, or other complications.
There are three main causes of immunodeficiency disorders...
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Nephrotic Syndrome I : Introduction

Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of fluid...

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Immune Profiling Identifies High-Risk Neutrophil-Rich Subtype in Checkpoint Inhibitor Nephritis.

Idris Boudhabhay1,2,3,4,5, Helene Lazareth3,6, Julie Oniszczuk7

  • 1Centre de Recherche des Cordeliers, Institut National de la Santé et de la Recherche Médicale, Sorbonne Université, Université de Paris Cité, Team Inflammation, Complement and Cancer, Paris, France.

Kidney International Reports
|February 23, 2026
PubMed
Summary
This summary is machine-generated.

Immune checkpoint inhibitor-induced acute interstitial nephritis (ICI-AIN) has distinct subtypes. A neutrophil-rich phenotype is linked to severe kidney injury, inflammation, and poorer outcomes, suggesting complement activation plays a role.

Keywords:
acute interstitial nephritischeckpoint inhibitorscomplementimmune phenotypingimmunotherapyneutrophil

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Area of Science:

  • Nephrology
  • Immunology
  • Oncology

Background:

  • Immune checkpoint inhibitor-induced acute interstitial nephritis (ICI-AIN) is a primary cause of acute kidney injury (AKI) in patients receiving immune checkpoint inhibitors (ICIs).
  • The underlying mechanisms of ICI-AIN, particularly the role of immune cell infiltrates, are not fully understood.
  • Characterizing these infiltrates is crucial for understanding ICI-AIN pathogenesis and improving patient outcomes.

Purpose of the Study:

  • To characterize immune cell infiltrates in kidney biopsies from patients with ICI-AIN.
  • To identify distinct ICI-AIN phenotypes based on immune cell composition.
  • To correlate these phenotypes with clinical presentation, severity of AKI, and response to therapy.

Main Methods:

  • Retrospective analysis of 49 biopsy-proven ICI-AIN cases.
  • Multiplex immunofluorescence was used to quantify various immune cells (macrophages, neutrophils, B cells, T cells, plasmocytes).
  • Unsupervised clustering identified patient subgroups, which were then correlated with clinical data and outcomes. The role of C5a/C5aR1 in neutrophil recruitment was also explored.

Main Results:

  • Three immune phenotypes were identified: low mononuclear, high mononuclear, and neutrophil-rich.
  • The neutrophil-rich cluster (cluster 3) showed significantly higher systemic inflammation, more severe initial AKI, and was marked by granular casts and neutrophilic tubulitis.
  • Steroid response rates were lower in the neutrophil-rich cluster (38%) compared to the high mononuclear cluster (93%), with more frequent relapses in cluster 3. Urine C5a correlated with neutrophil infiltration.

Conclusions:

  • Distinct ICI-AIN subtypes exist, with a neutrophil-rich phenotype associated with complement activation (C5a/C5aR1 pathway) and a poorer prognosis.
  • This neutrophil-rich phenotype is linked to increased inflammation, severe AKI, reduced response to steroids, and higher relapse rates.
  • These findings highlight the importance of immune cell profiling in ICI-AIN for refining diagnosis and tailoring treatment strategies.