Trophic factor and XXXX supplementation during cold storage rescue chronic renal injury.

@entity1707 @entity32 @entity82 @entity63 @entity39 @entity177 @entity204 @entity55910
PURPOSE: The use of organs from deceased after @entity204 and extended criteria donors grew in the last decade. These organs are more sensitive to @entity63 -reperfusion injury during transplantation and current preservation protocols do not protect them adequately. MATERIALS AND METHODS: In an autotransplanted, deceased after @entity204 donor @entity1707 kidney model we evaluated the benefits of supplementation with University of Wisconsin solution trophic factors and @entity55910 , an inhibitor of p38 mitogen-activated protein kinase. RESULTS: Supplemented solution improved renal recovery and limited @entity63 -reperfusion injury, particularly when agents were used in conjunction. Long-term benefits were highlighted by @entity177 , as determined by Picrosirius staining, and @entity32 , as evaluated by renal cell infiltration. Mechanistic evaluation showed decreased expression of epithelial-to-mesenchymal transition markers, a process involved in renal @entity82 development. Tumor @entity39 factor-a was markedly decreased in the treated experimental group. Apoptosis was also decreased, accompanied by decreased p38 mitogen-activated protein kinase phosphorylation. CONCLUSIONS: Supplementing the current gold standard kidney preservation protocol with trophic factors and p38 mitogen-activated protein kinase inhibitors markedly increased the quality of grafts in our @entity1707 deceased after @entity204 donor model. Hence, this represents a strategy of interest to improve transplantation outcomes.
