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Introduction Outcome after transplantation of kidneys derived from deceased brain death (DBD) donors is inferior compared to living donor kidneys. The aim of this study was to evaluate the effect of experimental brain death on immediate renal function. Secondarily, we tested the hypothesis that brain death results in acute renal inflammation and modulates renal metabolism. Materials & Methods Eight Danish landrace pigs served as DBD donors. After four hours of brain death, kidneys were removed and stored for 19 hours at 4°C in Custodiol® preservation solution, and then transplanted to eight recipients. Glomerular filtration rate (GFR) was defined as 51Cr-EDTA renal clearance. Systemic inflammation was studied by a plasma cytokine assay, while renal inflammation and changes in renal metabolism were measured by qRT-PCR. Results Directly following brain death GFR and urine output were reduced, while in the second hour hyperfiltration was observed. Subsequently, GFR and urine output decreased again. Free water clearance increased substantially following brain death indicating reduced vasopressin activity. No systemic inflammation was observed in the donors, while in recipients renal gene expression of IL-6, ICAM-1 and MCP-1, was increased ten hours post-reperfusion. Furthermore, DBD transplantation modulated renal gene expression of LDHA, PC and PCK-1 indicating changes in renal metabolism. Discussion In conclusion, brain death caused a triphasic response of GFR. No systemic inflammation in brain death donors was observed presumably due to active control of hemodynamics by fluid administration. I/R injury started to develop after reperfusion, as indicated by signs of mitochondrial dysfunction and renal inflammation, creating a window of opportunity for cytoprotective treatment early in the reperfusion phase