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Related Concept Videos

Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

858
Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
858
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

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Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
249

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Related Experiment Video

Updated: Jan 10, 2026

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection
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Spatial Transcriptomics Identify T Cell-Driven Mechanisms of Kidney Damage in Immune Checkpoint Inhibitor-Associated

Qian Qin1,2, Lennard Ostendorf1,2,3, Sophia L Wells4

  • 1Division of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA.

Biorxiv : the Preprint Server for Biology
|November 24, 2025
PubMed
Summary

Immune checkpoint inhibitor-associated acute interstitial nephritis (ICI-AIN) involves T cell infiltration. Spatial transcriptomics reveal CD8+ T cells drive inflammation via IFN-γ, impacting myeloid cells and kidney tubules in ICI-AIN.

Keywords:
ICI-AKIImmune Checkpoint InhibitorJAK-STAT1acute interstitial nephritisinterferon gammaspatial transcriptomics

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Area of Science:

  • Nephrology
  • Immunology
  • Spatial Biology

Background:

  • Immune checkpoint inhibitor-associated acute kidney injury (ICI-AKI) often presents as acute interstitial nephritis (ICI-AIN).
  • ICI-AIN is characterized by T cell infiltration and elevated CXCR3 ligands, but its inflammatory mechanisms remain unclear.

Purpose of the Study:

  • To compare the cellular composition and spatial organization of kidney tissue in ICI-AIN versus ICI-treated acute tubular necrosis (ICI-ATN).
  • To elucidate the cellular and molecular mechanisms driving inflammation in ICI-AIN using spatial transcriptomics.

Main Methods:

  • Applied sub-cellular spatial transcriptomics (Xenium Prime 5K) to 8 kidney biopsy specimens (4 ICI-AIN, 4 ICI-ATN).
  • Analyzed over 332,000 cells, identifying cellular niches and performing pathway and spatial crosstalk analyses.

Main Results:

  • Identified distinct fibrotic and inflammatory niches in ICI-AIN.
  • Observed increased interferon-gamma (IFN-γ)/STAT1 signaling in ICI-AIN.
  • Found CD8+ T cell infiltration and proinflammatory myeloid cells as dominant immune niches in ICI-AIN.
  • Demonstrated CD8+ T cell-derived IFN-γ likely drives myeloid cell inflammation and CXCL9/10/11 production.
  • Associated IFN-γ signaling with reduced oxidative phosphorylation in kidney tubular cells in ICI-AIN.

Conclusions:

  • Spatial transcriptomics provides novel insights into ICI-AIN pathophysiology.
  • IFN-γ-producing CD8+ T cells are identified as key drivers of ICI-AIN.
  • These CD8+ T cells represent potential future therapeutic targets for ICI-AIN.