B-Cell Activation in Acute Kidney Injury and Delayed Graft Function

M. Schiffer,¹ F. Wiehler,¹ R. Song,¹ R. Chen,¹ L. Schiffer,¹ M. Mengel,² H. Haller,¹ F. Gueler.¹

¹Nephrology, Hannover Medical School, Hannover, Germany
²Pathology, University of Alberta, Edmonton, Canada.

Meeting: 2015 American Transplant Congress

Abstract number: C21

Session Information

Session Name: Poster Session C: Antigen Presenting Cells in Alloimmune Responses/B Cells and Antibody in Alloimmune Responses

Session Type: Poster Session

Date: Monday, May 4, 2015

Session Time: 5:30pm-6:30pm

Presentation Time: 5:30pm-6:30pm

Location: Exhibit Hall E

Background:

Acute kidney injury (AKI) is a relevant complication after kidney transplantation and also after non-renal solid organ transplantation. Growing evidence points towards an important role of B-cells in acute kidney injury in the early phase of transplantation. Here we present evidence that due to ischemia reperfusion injury the chemokine CXCL13 is upregulated and B-cells are activated.

Methods:

AKI was induced by ischemia reperfusion injury (IRI) in two different mouse strains (C57Bl/6, CD1) by transient clipping of the renal pedicles for 35 min. Bilateral as well as unilateral clipping was performed. In addition, a kidney transplant model was performed with isogenic and allogenic kidney transplantation. In both models serial plasma samples were taken and ELISA for the B-cell-attracting chemokine 13 (CXCL13) was performed. mRNA tissue analysis for CXCL13, TNF-alpha, IL-6 and MCP-1 was done and renal morphology and leukocyte cell infiltration was characterized by histology and immunohistochemistry.

Results:

CXCL13 plasma levels increased within 24h after IRI and correlated with the extent of tissue damage and also with increased mRNA expression in renal tissue. CD-1 mice had more severe renal tissue damage and higher CXCL13 release than C57Bl/6 mice after 35min IRI. In AKI after kidney transplantation systemic CXCL13 release was potentiated in allogenic compared to isogenic kidney transplantation at 24h after transplantation and B- cells could be detected within 7 days after IRI in the tubulo-interstitial space.

Conclusion:

B-cell activation due to IRI is mediated by CXCL13 release. CXCL13 is a new creatinine independent biomarker for AKI and is useful also in unilateral renal damage detection. In the transplant setting blocking CXCL13 could be a novel target to prevent IRI induced B-cell infiltration.

To cite this abstract in AMA style:

Schiffer M, Wiehler F, Song R, Chen R, Schiffer L, Mengel M, Haller H, Gueler F. B-Cell Activation in Acute Kidney Injury and Delayed Graft Function [abstract]. Am J Transplant. 2015; 15 (suppl 3). https://atcmeetingabstracts.com/abstract/b-cell-activation-in-acute-kidney-injury-and-delayed-graft-function/. Accessed November 21, 2024.

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