ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: TH-PO012

S100A8/S100A9 Diminishes Acute Tubular Injury After Ischemia-Reperfusion

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Westhoff, Timm H., University Hospital Marien Hospital Herne, Herne, Germany
  • Seibert, Felix S., University Hospital Marien Hospital Herne, Herne, Germany
  • Schmidt-Ott, Kai M., Charite - Universitaetsmedizin Berlin, Berlin, Germany

Urinary calprotectin (S100A8/S100A9) has recently been identified as a promising biomarker in acute kidney injury (AKI). It is a mediator of the innate immune system and acts as a danger associated molecular pattern protein (DAMP). It remains elusive, however, whether calprotectin plays a pathophysiological role in AKI. Recently, there was first evidence that it might participate in the control of macrophage-mediated renal repair following ischemia/reperfusion. The present work examines whether calprotectin modulates acute I/R injury by means of a S100A9 -/- mouse model.


Since S100A8 -/- mice are not viable, S100A9 -/- knockout mice were established on a C57BL/6 background. I/R injury was induced by 25 min of unilateral ligation of the renal artery in S100A9 -/- and wildtype (WT) mice. The extent of tubular injury was assessed by a histological score and neutrophil gelatinase associated lipocalin (NGAL) and kidney injury molecule 1 (KIM-1) mRNA expression.


Histological tubular injury was comparable between S100A9 -/- and WT controls at 24h, while transition to fibrosis was aggravated in S100a9-/- mice. After 24h KIM-1 mRNA concentrations were higher in S100A9 -/- than in WT mice. The increase in NGAL mRNA expression was highly significantly larger in S100 A9 -/- than in WT mice at 24h. The difference of both KIM-1 and NGAL expression between the two mice strains disappeared by day 7. Sham operated animals did neither show any tubular injury nor an increase in KIM-1 or NGAL expression.


S100A9 deficiency is associated with increased I/R injury. Acting as an alarm signal, calprotectin may initialize tubular protective mechanisms after the induction of I/R.