Effects of brain death on stress and inflammatory response in the human donor kidney.
BACKGROUND: After kidney transplantation, a decreased graft survival is seen in grafts from brain dead donors compared to living donors, possibly related to a progressive inflammatory reaction in the graft. In this study, we focused on the effects of brain death on the inflammatory response (adhesi...
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| Format: | Conference item |
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2005
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| _version_ | 1797071489142358016 |
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| author | Nijboer, W Schuurs, T van der Hoeven, J Leuvenink, H van der Heide, J van Goor, H Ploeg, R |
| author_facet | Nijboer, W Schuurs, T van der Hoeven, J Leuvenink, H van der Heide, J van Goor, H Ploeg, R |
| author_sort | Nijboer, W |
| collection | OXFORD |
| description | BACKGROUND: After kidney transplantation, a decreased graft survival is seen in grafts from brain dead donors compared to living donors, possibly related to a progressive inflammatory reaction in the graft. In this study, we focused on the effects of brain death on the inflammatory response (adhesion molecules, leukocyte infiltration, and gene expression) and stress-related heat shock proteins in the human kidney. Research outcomes and clinical donor parameters were linked to outcome data after transplantation. METHODS: Human kidney biopsy specimens were obtained during organ retrieval from brain dead and living organ donor controls. On these specimens, immunohistochemistry and semiquantitative RT-PCR were performed. Regression analyses were performed connecting results to outcome data of kidney recipients. RESULTS: In brain death, immunohistochemistry showed an increase of E-selectin and interstitial leukocyte invasion versus controls; RT-PCR showed an increase of gene expression of HO-1 and Hsp70. One and 3 years after transplantation, high ICAM and VCAM expression proved to have a negative effect on kidney function in brain dead and living kidneys, while HO-1 proved to have a strongly positive effect, but only in kidneys from living donors. CONCLUSIONS: E-selectin expression and interstitial leukocyte accumulation in brain dead donor kidneys indicate an early phase inflammatory state prior to organ retrieval. Also, brain death causes a stress-related response resulting in upregulation of potentially protective heat shock proteins. The upregulation of HO-1 is beneficial in living donor kidneys, but might be inadequate in brain death. |
| first_indexed | 2024-03-06T22:54:00Z |
| format | Conference item |
| id | oxford-uuid:5fc28c5e-5767-47f1-8fcc-167ee7fd9419 |
| institution | University of Oxford |
| last_indexed | 2024-03-06T22:54:00Z |
| publishDate | 2005 |
| record_format | dspace |
| spelling | oxford-uuid:5fc28c5e-5767-47f1-8fcc-167ee7fd94192022-03-26T17:48:58ZEffects of brain death on stress and inflammatory response in the human donor kidney.Conference itemhttp://purl.org/coar/resource_type/c_5794uuid:5fc28c5e-5767-47f1-8fcc-167ee7fd9419Symplectic Elements at Oxford2005Nijboer, WSchuurs, Tvan der Hoeven, JLeuvenink, Hvan der Heide, Jvan Goor, HPloeg, R BACKGROUND: After kidney transplantation, a decreased graft survival is seen in grafts from brain dead donors compared to living donors, possibly related to a progressive inflammatory reaction in the graft. In this study, we focused on the effects of brain death on the inflammatory response (adhesion molecules, leukocyte infiltration, and gene expression) and stress-related heat shock proteins in the human kidney. Research outcomes and clinical donor parameters were linked to outcome data after transplantation. METHODS: Human kidney biopsy specimens were obtained during organ retrieval from brain dead and living organ donor controls. On these specimens, immunohistochemistry and semiquantitative RT-PCR were performed. Regression analyses were performed connecting results to outcome data of kidney recipients. RESULTS: In brain death, immunohistochemistry showed an increase of E-selectin and interstitial leukocyte invasion versus controls; RT-PCR showed an increase of gene expression of HO-1 and Hsp70. One and 3 years after transplantation, high ICAM and VCAM expression proved to have a negative effect on kidney function in brain dead and living kidneys, while HO-1 proved to have a strongly positive effect, but only in kidneys from living donors. CONCLUSIONS: E-selectin expression and interstitial leukocyte accumulation in brain dead donor kidneys indicate an early phase inflammatory state prior to organ retrieval. Also, brain death causes a stress-related response resulting in upregulation of potentially protective heat shock proteins. The upregulation of HO-1 is beneficial in living donor kidneys, but might be inadequate in brain death. |
| spellingShingle | Nijboer, W Schuurs, T van der Hoeven, J Leuvenink, H van der Heide, J van Goor, H Ploeg, R Effects of brain death on stress and inflammatory response in the human donor kidney. |
| title | Effects of brain death on stress and inflammatory response in the human donor kidney. |
| title_full | Effects of brain death on stress and inflammatory response in the human donor kidney. |
| title_fullStr | Effects of brain death on stress and inflammatory response in the human donor kidney. |
| title_full_unstemmed | Effects of brain death on stress and inflammatory response in the human donor kidney. |
| title_short | Effects of brain death on stress and inflammatory response in the human donor kidney. |
| title_sort | effects of brain death on stress and inflammatory response in the human donor kidney |
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