1. ¹Nephrology, Dialysis and Transplant Unit, Department of Emergency and Organ Transplantation, University of Bari, Bari, Italy
2. ²Renal Unit, Department of Biomedical Sciences, University of Foggia, Foggia, Italy
3. ³Urology and Transplant Unit, Department of Emergency and Organ Transplantation, University of Bari, Bari, Italy
4. ⁴Veterinary Unit, Department of Emergency and Organ Transplantation, University of Bari, Bari, Italy
5. ⁵Clinical Pathology Unit, Department of Biomedical Sciences, University of Foggia, Foggia, Italy

Correspondence: G Grandaliano, Nephrology, Dialysis and Transplant Unit, Department of Emergency and Organ Transplantation, University of Bari, Policlinico, Piazza Giulio Cesare 11, Bari 70124, Italy. E-mail: g.grandaliano@nephro.uniba.it

Received 30 January 2007; Revised 30 May 2007; Accepted 19 June 2007; Published online 8 August 2007.

Abstract

Delayed graft function (DGF) in kidney transplantation is associated with an increased risk of acute rejection. Myeloid dendritic cells (DCs) are involved in graft rejection, whereas plasmacytoid DCs may play a role in inducing tolerance. We evaluated the presence and phenotype of the DCs in renal graft biopsies of 15 patients with DGF collected before and 7–15 days after transplantation. Biopsies taken from normal patients and from transplant recipients with acute calcineurin inhibitors (CNIs) nephrotoxicity served as a control group. Specific markers of myeloid, plasmacytoid, and mature DCs were imaged by confocal microscopy and immunohistochemistry. In normal kidneys and pre-transplant biopsies, sparse niches of myeloid and plasmacytoid cells were found but these were significantly increased with few mature cells during DGF. This same pattern was seen in acute rejection but with overall higher cell numbers. In CNI nephrotoxicity, myeloid cells were slightly increased but plasmacytoid cells were significantly higher than in DGF. Using a pig model, we found that a short period of warm ischemia followed by reperfusion led to myeloid cell infiltration of the kidney. Our data suggest that ischemia-reperfusion injury may cause an imbalance between intragraft myeloid and plasmacytoid DCs, which might be related to DGF and acute rejection.