We read the article “Expression of IL-8 during reperfusion of renal allografts is dependant on ischemic time” by Araki et al. (1) with great interest. It raised a number of interesting issues. We were rather surprised by the high rate of delayed graft function (DGF) in living donors (4/20). No explanation has been given for this, or indeed any, comment. We are also unclear about the nephrectomy procedure carried out whether it was performed laparoscopically or by open technique. The warm ischemia in the living donor group is not known. It is possible the kidneys were harvested laparoscopically resulting in an increased warm ischemia time thus leading to a higher incidence of DGF (2). We were also surprised to see interleukin (IL)-8 levels similar in both living and cadaveric biopsies before reperfusion while CXCL 10/interferon gamma inducible protein (IP) -10 levels were higher in the cadaveric group. Since IP-10 was expressed initially in the cadaveric biopsies and there was also a thirteen fold rise in IL-8 after reperfusion suggests that sufficient stimulus for chemokine expression was present. Proinflammatory cytokines such as IL-1, tumor necrosis factor, and oxidative stress are known to induce NF-kB the key transcription factor that mediates IL-8 release (3–5). Failure in expression of monocyte chemoattractant protein (MCP)-1 and RANTES is quite understandable as their expression is delayed and sustained (6). Avneesh Kumar Abdul Hammad Rana Rustom Sir Peter Medawar Transplant Unit Royal Liverpool University Hospital Liverpool, UK