Oral Presentations: Basic Sciences II.
Mező, Blanka
Research Laboratory, 3rd Department of Internal Medicine, Semmelweis University
06704263308
mezoblanka@gmail.com
Determination of complement profile in kidney transplant recipients
Blanka Mező1, Dorottya Csuka1, Nóra Veszeli1, Tímea Gombos1, Andreas Heilos2, Krisztina Rusai2, Gregor Bond3, Farsad Eskandary3, Georg Böhmig3, Zoltán Prohászka1
1Research Laboratory, 3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary;
2Department of Paediatrics and Adolescent Medicine, Medical University Vienna, Austria, Vienna, Austria;
3Division of Nephrology and Dialysis, Department of Medicine III, Medical University Vienna, Vienna, Austria
molecular sciences
Oral Presentations: Basic Sciences II.
Doctoral School: Basic Medicine
Program: Clinical and Experimental Cardiology / Atherosclerosis
Supervisor: Zoltán Prohászka
E-mail address: mezoblanka@gmail.com
Introduction: Antibody mediated rejection (ABMR) is a severe clinical problem which is the major immunological cause of kidney transplant failure. According to current knowledge, late ABMR is classically caused by the development of donor specific antibodies (DSA) and the complement system believed to contribute to tissue damage. The aim of this work was to determine the levels of several complement proteins, regulators and activation products in kidney transplant recipients.
Methods: In the present study, 741 long-term transplant patients subjected to cross sectional ABMR screening. Our analysis focused on 106 patients having detectable DSA in their serum and for comparative analysis, 106 DSA negative patients were selected. The levels of complement activation products (C3a, SC5b-9, C4d and Bb) were measured by enzyme-linked immunosorbent assay (ELISA) using EDTA plasma and urine samples. The activity of the alternative and MBL pathways were also measured by ELISA. The classical pathway activation was screened by CH50 hemolytic assay. Radial immunodiffusion was used to determine the concentration of factor I (FI) and factor B (FB).
Results: Complement profile was compared between the DSA positive and negative groups. The activity of the MBL pathway was significantly decreased in the DSA+ group (p<0.0001). No other significant difference was observed in the plasma/urine levels of complement activation products and the concentration of FI and FB. Neither the alternative nor the classical pathway activity was significantly different.
Conclusion: Our results suggest that the MBL pathway may play a role in the pathomechanism of ABMR. Further analysis is necessary to identify association of complement activation with signs of ABMR in these patients.
This work was supported by the National Research Fund of Hungary (NN110909).
Szabad
nem rendelkezett róla
1199
Blanka Mező1, Dorottya Csuka1, Nóra Veszeli1, Tímea Gombos1, Andreas Heilos2, Krisztina Rusai2, Gregor Bond3, Farsad Eskandary3, Georg Böhmig3, Zoltán Prohászka1
1Research Laboratory, 3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary;
2Department of Paediatrics and Adolescent Medicine, Medical University Vienna, Austria, Vienna, Austria;
3Division of Nephrology and Dialysis, Department of Medicine III, Medical University Vienna, Vienna, Austria