Aggravation of fibrin deposition and microthrombus formation within the graft during kidney transplantation
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Updated: Oct 19, 2025

Mouse Kidney Transplantation: Models of Allograft Rejection
Published on: October 11, 2014
Tamar A J van den Berg1,2, Marius C van den Heuvel3, Janneke Wiersema-Buist4
1Department of Surgery, University Medical Center Groningen, University of Groningen, P.O. Box 30 001, 9700 RB, Groningen, The Netherlands. pol.chirurgie@gmail.com.
Abstract:
In kidney transplantation, microthrombi and fibrin deposition may lead to local perfusion disorders and subsequently poor initial graft function. Microthrombi are often regarded as donor-derived. However, the incidence, time of development, and potential difference between living donor kidneys (LDK) and deceased donor kidneys(DDK), remains unclear. Two open-needle biopsies, taken at preimplantation and after reperfusion, were obtained from 17 LDK and 28 DDK transplanted between 2005 and 2008. Paraffin-embedded sections were immunohistochemically stained with anti-fibrinogen antibody. Fibrin deposition intensity in peritubular capillaries(PTC) and glomeruli was categorized as negative, weak, moderate or strong and the number of microthrombi/mm2 was quantified. Reperfusion biopsies showed more fibrin deposition (20% to 100% moderate/strong, p < 0.001) and more microthrombi/mm2 (0.97 ± 1.12 vs. 0.28 ± 0.53, p < 0.01) than preimplantation biopsies. In addition, more microthrombi/mm2 (0.38 ± 0.61 vs. 0.09 ± 0.22, p = 0.02) and stronger fibrin intensity in glomeruli (28% vs. 0%, p < 0.01) and PTC (14% vs. 0%, p = 0.02) were observed in preimplantation DDK than LDK biopsies. After reperfusion, microthrombi/mm2 were comparable (p = 0.23) for LDK (0.09 ± 0.22 to 0.76 ± 0.49, p = 0.03) and DDK (0.38 ± 0.61 to 0.90 ± 1.11, p = 0.07). Upon reperfusion, there is an aggravation of microthrombus formation and fibrin deposition within the graft. The prominent increase of microthrombi in LDK indicates that they are not merely donor-derived.
Insights
Microthrombi and fibrin deposition increase after kidney transplant reperfusion. This suggests microthrombi in living donor kidneys (LDK) are not solely donor-derived, impacting graft function.
Area of Science:
- Nephrology
- Transplantation immunology
- Vascular pathology
Background:
- Microthrombi and fibrin deposition in kidney grafts can impair initial function.
- These microthrombi are often presumed to be donor-derived.
- The timing and origin differences between living donor kidneys (LDK) and deceased donor kidneys (DDK) remain unclear.
Purpose of the Study:
- To investigate the incidence and development of microthrombi and fibrin deposition in kidney transplants.
- To compare these findings between LDK and DDK.
- To determine if microthrombi are exclusively donor-derived.
Main Methods:
- Two biopsies (preimplantation and post-reperfusion) from 17 LDK and 28 DDK.
- Immunohistochemical staining for fibrinogen.
- Quantification of microthrombi and fibrin deposition intensity in glomeruli and peritubular capillaries.
Main Results:
- Post-reperfusion biopsies showed significantly increased fibrin deposition and microthrombi compared to preimplantation biopsies.
- Preimplantation DDK had more microthrombi and greater fibrin intensity than LDK.
- Post-reperfusion, microthrombi counts became comparable between LDK and DDK.
Conclusions:
- Reperfusion significantly aggravates microthrombus formation and fibrin deposition in kidney grafts.
- The substantial increase in microthrombi in LDK post-reperfusion challenges the notion that they are solely donor-derived.
- These findings highlight the importance of post-transplant events in graft microvascular injury.
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