Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.657852
Title: Angiogenesis in human parathyroid disease and chronic allograft nephropathy
Author: Mitchell, D.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 2007
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Abstract:
Here we have demonstrated evidence of an angiogenic switch that occurs in human parathyroid tissue when diseased. Our data have not shown a significant expression of VEGF in these samples. A hallmark of chronic allograft nephropathy (CAN) is endothelial cell damage, resulting in hypoxia, providing a stimulus for angiogenesis, or new vessel formation. This study aims to compare vascularity of kidneys with CAN versus normal. In addition, validation of renal biopsy samples in the assessment of angiogenesis has been performed. CD31 staining from CAN nephrectomies exhibited diminished cortical and medullary staining and was accompanied by a significant increase in proliferation index when compared with normal. There was significant correlation in MVCs in core biopsies and the corresponding kidney cross-section. Early biopsies from grafts which developed CAN show significantly higher MVCs compared with the corresponding nephrectomy. The number of proliferating ECs was significantly increased in this biopsy group compared with normal kidney. Early protocol biopsies from grafts which developed CAN showed significantly higher MVCs compared with those with stable graft function (p=0.0002). This study demonstrates reduced density of CD31-positive microvessels in CAN compared with normal. In addition, the investigation of changes in the microvasculature in CAN by study of core biopsies has been validated and confirms preservation of normal vasculature in early CAN. Together, with evidence of proliferating endothelial cells these findings support a hypothesis that, early in the development of CAN, angiogenesis is stimulated, but that, despite this attempt at tissue repair, progressive microvascular loss results in interstitial fibrosis and eventual organ failure.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (M.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.657852  DOI: Not available
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