Innate immunity in donor procurementCheung, Kitty P.; Kasimsetty, Sashi G.; McKay, Dianne B.Current Opinion in Organ Transplantation: April 2013 - Volume 18 - Issue 2 - p 154–160 doi: 10.1097/MOT.0b013e32835e2b0d ORGAN PRESERVATION AND PROCUREMENT: Edited by Ernest van Heurn Buy Abstract Author InformationAuthors Article MetricsMetrics Purpose of review Ischaemic kidney injury occurs during organ procurement and can lead to delayed graft function or nonviable grafts. The innate immune system is a key trigger of inflammation in renal ischaemia. This review discusses the components of innate immunity known to be involved in renal ischaemic reperfusion injury (IRI). Understanding how inflammatory damage is initiated in renal IRI is important for the development of targeted therapies aimed at preserving the donor organ. Recent findings Much remains to be determined about the role of innate immune signalling in renal ischaemia/reperfusion injury. Recently, discoveries about complement receptors, Toll-like receptors (TLRs), NOD-like receptors (NLRs) and inflammasomes have opened new avenues of exploration. We are also now learning that macrophages, complement and TLR activation may have additional roles in renal repair following IRI. Summary A greater understanding of the mechanisms that contribute to innate immune-mediated renal ischaemic damage will allow for the development of therapeutics targeted to the donor organ. New data suggest that treatment limited to specific receptors on specific cells, or localized to specific regions within the kidney, may provide novel approaches to maximize our use of donor organs, particularly those that may have been discarded due to prolonged preimplantation ischaemia. Division of Nephrology and Hypertension, Department of Medicine, University of California at San Diego, La Jolla, California, USA Correspondence to Dianne McKay, MD, Division of Nephrology and Hypertension, Department of Medicine, University of California at San Diego, 9500 Gilman Drive #621, La Jolla, CA 92093, USA. Tel: +1 858 246 1251; fax: +1 858 246 1191; e-mail: email@example.com © 2013 Lippincott Williams & Wilkins, Inc.