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Chronic epithelial kidney injury molecule-1 expression causes murine kidney fibrosis

Benjamin D Humphreys1, Fengfeng Xu, Venkata Sabbisetti

  • 1Renal Division, Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA. bhumphreys@partners.org

The Journal of Clinical Investigation
|August 28, 2013
PubMed

Insights

Kidney injury molecule-1 (KIM-1) promotes kidney fibrosis and chronic kidney disease progression. Sustained KIM-1 expression links acute kidney injury to progressive renal failure, offering a potential therapeutic target.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pathology

Background:

  • Acute kidney injury (AKI) increases risk for chronic kidney disease (CKD) and end-stage renal failure.
  • The molecular mechanisms linking AKI to CKD are not fully understood.
  • Kidney injury molecule-1 (KIM-1) is an epithelial phosphatidylserine receptor expressed after kidney injury.

Purpose of the Study:

  • To investigate the role of KIM-1 in promoting kidney fibrosis and CKD.
  • To elucidate the molecular pathways by which KIM-1 contributes to renal disease progression.

Main Methods:

  • Conditional expression of KIM-1 in renal epithelial cells (Kim1(RECtg)) in mice.
  • Analysis of kidney histology, function, and molecular markers in Kim1(RECtg) mice.
  • In vitro studies using immortalized proximal tubule cells expressing KIM-1.
  • Assessment of experimental kidney fibrosis in mice with mutant KIM-1.

Main Results:

  • Kim1(RECtg) mice developed spontaneous, progressive interstitial kidney inflammation and fibrosis, leading to renal failure.
  • Elevated monocyte chemotactic protein-1 (MCP-1) expression was observed in Kim1(RECtg) kidneys.
  • KIM-1 expression triggered MCP-1 secretion and enhanced macrophage chemotaxis in vitro.
  • A mutant, truncated KIM-1 ameliorated experimental kidney fibrosis and reduced MCP-1 levels.

Conclusions:

  • Sustained KIM-1 expression promotes kidney fibrosis and progression to chronic kidney disease.
  • KIM-1 acts via MCP-1 to drive inflammation and fibrosis, linking acute injury to progressive renal failure.
  • KIM-1 represents a potential therapeutic target for preventing CKD progression after AKI.

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