B-Cell Activation in Acute Kidney Injury and Delayed Graft Function
1Nephrology, Hannover Medical School, Hannover, Germany
2Pathology, University of Alberta, Edmonton, Canada.
Meeting: 2015 American Transplant Congress
Abstract number: C21
Keywords: B cells, Graft function
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 May 16, 2025.« Back to 2015 American Transplant Congress