• Simona Oltean, Rille Pullerits, Anne Flodén, Michael Olausson, and Mihai Oltean.
• The Transplant Institute, Sahlgrenska University Hospital, Gothenburg 41345, Sweden. mihai.oltean@surgery.gu.se.
• J Transl Med. 2013 Jan 1; 11: 233.

IntroductionResistin increases during several inflammatory diseases and after intracerebral bleeding or head trauma. Resistin activates the endothelium and may initiate an inflammatory response. No data are available on resistin in brain dead donors (DBD) that regularly manifest a pronounced inflammatory state.MethodsWe analyzed plasma resistin in 63 DBDs and correlated results with donor variables and the postoperative course following kidney transplantation using organs from these donors. Endocan and monocyte chemotactic protein (MCP)-1 were also studied. Twenty-six live kidney donors (LD) and the corresponding kidney transplantations were used as controls.ResultsDBDs had higher resistin (median/range 30.75 ng/ml, 5.41-173.6) than LD (7.71 ng/ml, 2.41-15.74, p < 0.0001). Resistin in DBD correlated with delayed graft function (DGF) in the kidney recipients (r = 0.321, p < 0.01); receiver operating characteristic curve revealed an area under the curve of 0.765 (95% confidence interval [CI] 0.648-0.881, p < 0.01) and a cut-off value for resistin of 25 ng/ml; MCP-1 and endocan were higher in DBDs (p < 0.0001) but did not correlate with DGF or acute rejection. No relationship was found between the studied molecules and the postoperative course of LD kidney transplants.ConclusionsHigh resistin levels in the DBD before organ retrieval are associated with DGF after kidney transplantation. The resistin increase seems related to the inflammatory state after brain death but not to the cause of death.

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